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Some Effects of Environmental Pollution on Development of Infants

 

Summary

(Citations of sources, and the full text, will follow this summary)

 

Section 1. (summary)  There have been large increases in major non-communicable, long-term disorders, including neurological conditions, among American children in recent decades, beginning in the 1960’s and ‘70’s;  this is according to U.S. government statistics and highly-published researchers. Those disorders have affected males principally; aside from diagnosed disorders, there have also been adverse developments among boys and young men in the general population as well. Since genetics could not change so quickly, the origins of the increasing disorders and adverse trends are almost certainly to be found in environmental exposures, probably in conjunction with varying genetic susceptibilities to effects of the toxins.  Toxins present in food are a very important form of such exposure.  (The full text, including references to authoritative sources, is in Section 1)

 

Section 2. (summary) 

Section 2.a (summary)Vulnerability of the brain’s development to toxins in the early period after birth:

Many authoritative sources (EPA, NIH, U.S. ATSDR, leading scientists, a council of the U.S. National Academies, WHO, etc.) recognize the early-postnatal period as being a time of vulnerability to effects of environmental toxins, because of the major development taking place after birth. Development of the brain (see preview charts below) is known to be vulnerable to effects of toxins during the period when the developmental processes are active.                 

 

Fig. 1:  Brain development, preview

 

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There is good reason to see the postnatal period as often being a time of greater vulnerability than the prenatal period, based on

  a) over thirty studies that have found greater effects of toxins during the postnatal period than prenatally,

  b) a clear EPA statement saying that the postnatal period is the time of greatest sensitivity to a serious neurodevelopmental toxin (PBDEs), which increased dramatically in humans in the late 20th century, and

  c) the expert generalization, with considerable support, that exposures of the developing brain to a major class of toxins after birth are 10 to 20 times higher than before birth.

(Full text, including references to authoritative sources, in Section 2.a)

 

Section 2.b (summary):  Exposures to developmental toxins are far greater postnatally than prenatally, according to highly-authoritative sources and many studies.

 

Section 2.c (summary):   The vulnerability to developmental toxins of concern here is to toxins to which most infants are exposed, at environmental background levels. 

 

Section 2.d (summary):   The early months after birth are likely to be the period most vulnerable to developmental toxins, as indicated by considerable evidence.  

 

Section 2.e (summary):    Several studies have found associations of postnatal exposures with autism prevalence, including in dose-response relationships

 

 

 

Section 3. (summary)   Quoting a 2004 expert statement concerning environmental toxins that can affect development:  "these substances have caused contamination of human milk only during the last half century, and long-term health impacts are now being discovered."  The State of Washington Department of Ecology considers breastfed infants to be at the very highest level of exposure to these toxins, sharing that top position with only two other groups, both of which are groups that have unusually high exposures to contamination or industrial pollution.  (Full text, including references to authoritative sources, at Section 3.a)

 

There is considerable scientific evidence indicating that these toxins, at common levels of exposure, can cause adverse effects in children.  Four different developmental toxins have each been found to be typically present in human milk in concentrations greatly exceeding established safe levels, while infant formula has been found to have very little or no detectable concentrations of those toxins. (many sources cited)

 

Figure  3, preview

 

Shown below are observed effects on 9-year-old children of fairly common developmental exposures to PCBs.

(Note that the bottom lines are not at 0)

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http://www.pollution-effects.info/index_files/image021.gifSection 3.a (summary):  PCBs have been found in many human and animal studies to “impact normal brain development,” at levels to which humans are very often exposed; specific effects observed have included distractibility, reduced IQ, and poor memory and school performance; PCBs have been found to be present in human milk in doses 63 to 270 times the minimal risk level established by the U.S. Agency for Toxic Substances and Disease Registry, and essentially absent in infant formula.

  (Full text, including references to authoritative sources, at Section 3.a)

 

 

A scientist who is a member of both the U.S. National Academy of Sciences and the Institute of Medicine stated after completion of a laboratory experiment, “If human fetal and infant effects parallel rat impacts, we would predict that there would be a correlation between the PCB/PBDE levels in human breast milk and in infant blood with the probability of autism onset.” 

 

 

There is considerable evidence indicating that postnatal exposure to PCBs is more harmful than prenatal exposure. 

 

 (Full text, including references to authoritative sources, at Section 3.a)

 

Section 3.a.2:  Substantial evidence also indicates that, following developmental exposure to various toxins, including PCBs, dioxins and mercury, adverse effects are often only found well past early childhood.  Long latencies before effects of toxic exposures are observed, lasting years or even decades, are well established.

 

 (Full text, including references to authoritative sources, at Section 3.a.2)

 

Section 3.a.3:  Various studies have failed to find adverse effects of the developmental toxins in human milk when testing children in early childhood.  Given the contents of Section 3.a.2, one may wonder whether it is sensible to say something about failure to find adverse effects in early childhood as if that is all that matters, while saying nothing about the negative long-term effects.

 

 

Section 3.b (summary):  Brominated flame retardants, which include PBDEs and HBCD, are recognized neurodevelopmental toxins.

-- There have been high and increasing levels in breast milk of HBCD, which the EPA has designated as a “High hazard” for developmental neurotoxicity; levels have been found to be thousands of times higher in some homes than in others, with higher human exposures found to be associated with presence of typical electronic devices and carpeting.

Preview of Fig. 5.1

image044.gif-- There have been ongoing high lactational exposures to PBDEs, at levels over ten times higher than a few decades ago; effects of PBDE exposure, including at human background levels, have been found to include developmental neurotoxicity, hyperactivity, learning disability, memory defects, and poor social competence.

 

-- The EPA says that sensitivity to this toxin is greatest postnatally.

 

(Full text, including references to authoritative sources, at Section 3.b)

 

 

 

Section 3.c (summary):  According to a major toxicology textbook, dioxins can have “particularly devastating” effects on development, and children are most susceptible to them during development and nursing.  Dioxin levels have also been associated with harmful neurological effects at ages 12 to 15, including as related to attention deficits and learning disability; and those effects were linked with elevated levels of dioxin that are very common within the general population. Breastfeeding has been found in studies to have been the main determinant of long-term levels of that toxin.  (Full text, including references to authoritative sources, at Section 3.c)

 

 

Section 3.d (summary):  Mercury is a known neurodevelopmental toxin that often already exceeds the established safe level in infants at birth, and then a very large part of a mothers’ long-term accumulation of that chemical is usually rapidly transferred to an infant in breast milk;  “clearly documented toxic effects (of mercury) on the immature brain” are authoritatively recognized to be able to occur well into the postnatal period.  One of the many different forms of mercury has been found not to cause autism, whereas mercury in general has been closely associated with autism, in many studies.  In a 2013 study by a team of 12 researchers, levels of several metals including mercury were found to be associated with autism and were also “strongly associated with variations in the severity of autism;" mercury was the variable that was “most consistently significant” in relation to autism in both red blood cells and whole blood.  (Full text, including references to authoritative sources, at Section 3.d)

 

Section 3.e:  (Summary):  Pesticides and lead have been found to be extensively present in human milk and undetectable in infant formula in the U.S., in recent authoritative studies. (Full text or references to full text and sources at Section 3.e)

 

Section 3.e.2: (Summary):  Lead:  "No amount of lead exposure is safe," according to impeccable authority.  It is probable that a present-day American infant's lead levels would be predominantly determined by breastfeeding (or not breastfeeding).  Sources of lead in women, and therefore in breast milk, include occupational and hobby exposures, cosmetics, common foods, local and regional industrial pollution, and many other sources. (Full text, including references to authoritative sources, at Section 3.e.2)

   

3.e.2.c Effects of lead, even at very low doses

 

3.e.2.d: (Summary): Lead accumulates in the body over the long-term, and is mobilized during lactation

  

3.e.2.e:  (Summary): Major, rapid transfers take place from a grown person's lifetime accumulation of lead to small, developing infants:  In a study of 530 women at ages 65 to 87, having breastfed was still associated with an average 11% reduction in the women's lifetime accumulations of lead.  

 

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3.e.2.f (Summary): Higher-than-average childhood exposures to lead have been found to be very measurably linked with changes in brain volume in adulthood.

 

 

3.e.2.g (Summary):  Lead is especially likely to have its harmful effects during the early postnatal period.

 

3.e.2.h:  (Summary):  Many studies have found associations between lead and mercury exposure and autism, including at levels found in a very significant minority of U.S. children.

 

3.e.2.i:  (Summary):  Many studies have shown that ADHD is associated with lead at levels found in many tens of thousands of U.S. children.

 

  

Section 4. (summary):  Several studies have found prevalence of neurological disorders to correlate with breastfeeding:

 Section 4.a.1:  Direct Links:

Four studies published in 2009 and later have found positive correlations between breastfeeding duration and autism prevalence, in dose-response relationships.  One of those studies investigated data from all 50 U.S. states and 51 U.S. counties and found 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."  (full text, including references to sources, at Section 4.a)

 

Section 4.a.2:  Studies that indirectly link breastfeeding with risk of autism:

 

Section 4.a.2.1:  Emissions from municipal incinerators were found to be closely associated with all four adverse neurological outcomes that were investigated in young children who had been breastfed, and effects found in children in the general population with similar exposures were far smaller.  The results indicating unfavorable associations with history of breastfeeding were mostly concealed, in this study.

 

Section 4.a.2.2. Typical breast milk is the predominant source to infants of pesticides, which in turn are closely associated with autism.  There are good reasons to see breastfeeding as the predominant pathway for exposure of infants to those pesticides. (Full text, including references to authoritative sources, at Section 4.a.2.2)

 

 

Section 4.b:  Other studies have found two substantial, parallel declines according to birth order:  autism incidence, and concentrations of toxins in breast milk. (see chart and caption below)  Those two declines’ taking place in parallel might not be coincidence. (Full text, including references to authoritative sources, at Section 4.b)

 

Preview of Fig. 6.a

Concentrations of lipophilic chemicals in human milk decline with additional births, as the mother’s long-term accumulations are excreted in the milk.  It is known that some of those chemicals are neurodevelopmental toxins.

 

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Odds of a child’s having autism also decline greatly with birth order, for unknown reasons.

 

But some people might see a logical connection between the decline in autism with birth order and the decline in developmental toxins ingested (see above) in relation to birth order.

 

 (Full text, including references to sources, at Section 4.b)

 

Section 4.c:  Studies that have associated autism with less breastfeeding

 

 Fig. 7, preview

image046.gifSection 5. (summary):  There have been major increases in breastfeeding, which paralleled the major increases in disorders in children; increases in breastfeeding were rapid for a decade or so beginning in the early 1970's and slower later, and increases in disorders followed a similar pattern.  The increases in relation to the 1970 rate were especially dramatic in the case of longer-term breastfeeding

In addition to major increases in what is probably the predominant pathway of developmental toxins to infants (breastfeeding -- see Section 6 just below), concentrations of some major toxins (brominated flame retardants) were also rapidly increasing in the environment and in human milk during recent decades. (Full text, including references to authoritative sources, at Section 5)

 

 

 

Section ­6. (summary):  Breastfeeding may be a unique pathway of widespread infant exposure to developmental toxins in doses exceeding established safe levels.  Scientists who should know about developmental toxins apparently do not know of any other toxins to which infants or fetuses are widely exposed in doses exceeding established safe levels, aside from the four developmental toxins that are transferred in high concentrations via breastfeeding. (Full text at Section 6)

 

 

 

Section 7. (summary):  Far more young males than young females have been diagnosed in recent decades with certain neurological disabilities, including ADHD and ASD.  In addition, boys and young men in general have been falling behind in educationThere has been nothing but speculation as to the causes of these relatively recent adverse developments among young males.

 

 Preview of Figure 7.a

image024.gifRelevant to the above, remember from Section 3 that developmental exposures to the specific toxins discussed there have all been associated with one or more of the following:  learning disability, attention deficits, hyperactivity, and autism.

 

In addition, developmental exposures to those toxins have been linked in many studies with later symptoms of most of those impairments very disproportionately in young males. 

 

Those toxins, with their apparent male-adverse effects, are all high in human milk and very low in the alternative infant feeding. (see Section 3)   As indicated in Section 5, breastfeeding rates -- and therefore infant exposures to those toxins -- were increasing rapidly at a time that is fully compatible with developmental origins of the increases in disorders in young males.

 

The tracking of increases in disorders with breastfeeding increases could be dismissed as coincidence except for the fact that human milk has been authoritatively determined to have distinctively high levels of certain toxins, toxins that have been linked in many studies with neurological impairments specifically in males.

 

 

(For the full text, including references to authoritative sources, see Section 7)

 

7.a  (summary):  Environmental toxins discussed here (PCBs, dioxins, mercury, lead, and certain pesticides) have been found in scientific studies to have sex-specific adverse effects on males in the following respects:  capacity for higher cognitive processes, structure of the brain, volume of the brain, and development in motor and social areas. (Full text, including references to authoritative sources, at Section 7.a)

 

When seeing apparent effects (below) of mercury exposure on males in a general population of children who consume above-average amounts of fish, bear in mind the large amount of transfer of mercury that takes place via human milk (see Section 3.d) at a stage when the developing brain is especially vulnerable (Section 2).

Preview of Fig. 6

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Shown above are two out of six charts provided in the study that showed similar results of many tests, all indicating very much the same negative associations of mercury levels with scholastic achievement of males.

 

 

7.b  (summary):  In addition to the direct associations described above, these toxins have also been found to be linked with adverse neurological outcomes specifically on males via reduction of certain hormones, including testosterone. Testosterone has a major role in promoting neurological development and is also important to male motivation and attention. (Full text, including references to authoritative sources, at Section 7.b)

 

7.b.1:  Effects of dioxins have been found to include testicular atrophy as well as reduction of testosterone levels.  Substantial evidence also indicates that attention deficits and long-term reduced motivation are likely outcomes of dioxin exposure. (Full text, including references to authoritative sources, at Section 7.b.1)

 

 Figure 6.b.1, previewimage030.gif

7.b.2:   A 2014 American study found that a 10% increase in PCB levels in adolescent human males was associated with a 5.6% decline in their testosterone levels.  Observe in this chart the large increases in PCB levels that can occur during breastfeeding, with implications of resulting large corresponding reductions in testosterone levels.  (Full text, including references to authoritative sources, at Section 7.b.2)

 

7.b.3PBDEs, also, affect male hormones including testosterone, with outcomes including hyperactivity.

 

7.b.4:  Estradiol, a hormone that is neurodevelopmentally important for both sexes, is reduced by PCBs and PBDEs but much more so in males than in females.  (Full text, referring to authoritative sources, in Appendix E)

 

 

7.c:   The above toxins may well be the only developmental toxins (aside from lead, discussed in Section 3.e, and pesticides, discussed in Section 8.c) that have been found to have adverse neurological effects specifically on males, while having less or no effects on females. All of them widely reach infants in high doses by way of breastfeeding, and apparently do not widely reach infants in high doses by any means other than breastfeeding. (Full text, including references to authoritative sources, at Section 7.c)

 

 Preview of Figures 8 and 8.a

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7.d:  There is close historical parallel of increases in breastfeeding with births of males who will later have increasing problems associated with testicular dysfunction. This might not be coincidental, given the evidence in Section 7.b about effects of toxins in breast milk as related to testicular atrophy and testosterone reduction.  (Full text, including references to authoritative sources, at Section 7.d)

 

Declines in testicular function would be expected to lead to deficits in the male hormones that are important to attention and motivation. 

 

 

 

 

 

Section 8: (summary):  Developmental vulnerability to effects of pesticides is authoritatively recognized to be especially high postnatally.

8.a: (summary):  Human milk in developed as well as developing countries has been found to normally contain many pesticides. Infant formula in the U.S. has been authoritatively found to contain essentially no detectable pesticides.  (Full text, including references to authoritative sources, at Section 8.a)

 

8.b.1: (summary):  Although not ordinarily used in developed countries currently, DDT is still widely used in the developing world and (as a result) is present in a high percentage of fruits, vegetables, farmed seafood, and other foods commonly consumed in developed countries.  In a 2007 study, autism prevalence was found to be six times as high as normal near California agricultural fields where pesticides related to DDT were applied, and it varied in correlation with distance from the fields and with poundage of pesticides applied; the time of peak correlation of pesticide exposure with autism incidence was found to be in the year after birth. (Full text, including references to sources, at Section 8.b)

 

 

 Preview of Fig. 9

Correlation between DDT in human milk and test scores in 10 countries and 14 German states

 

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Exposures to the pesticides that have replaced DDT in developed countries also correlate with reduced IQ.

 

Section 8.b.2:   Pesticide exposure is associated with ASD prevalence.

 

Section 8.b.3:  There are many reasons to see breast milk as being the predominant source of pesticides to infants during the period of rapid brain development.  (For details and sources, see Section 8.b.3: )

 

8.c: (summary):  Pesticides have also been found to have adverse effects on males, specifically.  A study published in 2016 found very unusually high ratios of  adverse effects of common pesticides on motor and social developments of boys, with little or no adverse effects on girls.  (Full text, including references to sources, at Section 8.c)

 

 

 

Section 9: (summary): 

 The time when toxic exposures take place is critical in determining their effects; vulnerability is greatest when development is active.

 

 

  Fig. 11

 

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Those early months are the vulnerable developmental period for the functions that have become so increasingly impaired.

  

Breastfeeding, transferring six different developmental toxins to infants, each in very significant amounts, is by far most prevalent during the early months after birth; also, the concentrations of some of those toxins are apparently much higher during earlier breastfeeding. The combination of the above, together with the lactational effect of concentrating toxins in the milk (Section 2.b), leads to far greater total transfers of toxins soon after birth than at any other stage of development. The feeding type that is at the base of those high early-postnatal transfers went through very major increases in the late 20th century, in the U.S. and many other countries. (For full text including citations of authoritative sources, see Section 9.)                                                                                                                                                                                                                                                                                             

 

 

We should consider the possibility of a connection between

(a) the very large increases that have taken place in infants' exposures to toxins during the early months after birth as described above, and

(b) the concurrent, unexplained major growth in impairments in specific functions that are especially vulnerable to toxins during the early postnatal period.

 

Section 9.b:  In those same early-postnatal months, other neurological development is also taking place that has also not been going well during the period of major increases in breastfeeding; functions that are developing in those months include areas of attention, speech, gaze control, and many other areas.

 

 

Section 10: (summary):  The above points (to be presented in more complete form in the full text that follows this section, with references to sources) will then bring us to an important question:

 

Considering that

  (a) non-communicable disorders have been greatly increasing among children in recent decades -- for basically unknown reasons (Section 1),

  (b) the developmental processes taking place after birth are authoritatively recognized to be vulnerable to toxins ingested postnatally (Section 2),

  (c) toxins known to be typically at high levels in human milk have been found to lead to effects similar to symptoms of the increasing disorders (Section 3); and 

  (d) positive dose-response relationships have been found between breastfeeding and autism, in several published studies (Section 4),

 

 

it is reasonable to ask the following question of the medical organizations that promote breastfeeding:

 

How has it been determined that increasing exposures to developmental toxins in human milk (Figures 7 and 8a) have not been causing increases in disorders that outweigh the benefits of breastfeeding?

 

 

The U.S. medical associations that promote breastfeeding (pediatricians, family physicians and obstetricians and gynecologists) do not respond after being repeatedly asked the above question, with minor variations. They do not deny the presence of high levels of developmental toxins in human milk. And they do not deny the validity of the evidence indicating that those toxins, at levels such as in breast milk, can have adverse effects.

 

Since there is substantial peer-reviewed scientific evidence to support (a) through (d) above, it would seem to be appropriate for those physicians’ organizations to consider that evidence before they recommend feeding infants a food that has been authoritatively determined to contain several developmental toxins in concentrations far exceeding established safe levels. That kind of consideration of evidence would be especially called-for now that major, unexplained increases in child neurological disorders have followed the major increases in breastfeeding. (see Sections 1 and 5.)  And a response to the above question would be even more in order considering the apparent absence of known, widespread infant exposure of infants, by any pathway other than breastfeeding, to developmental toxins in doses exceeding established safe levels (see Section 6).

 

If careful study had been carried out on such an important matter of public health, a written record of the analysis of the important evidence ought to be available to the public. But there appears to be no such record available from any of the organizations that promote breastfeeding, which implies that the breastfeeding recommendations may be based on something other than careful consideration of the important evidence.

 

The promoters of breastfeeding point out that many studies have found that breastfeeding is associated with beneficial outcomes.  But, according to former U.S. Surgeon General Regina Benjamin, essentially all of those studies have been observational studies.  That is a study type that the leading authorities on medical evidence consider to be of low quality, highly subject to error. 

  (Full text, including references to authoritative sources, in Section 10)

 

 Preview of Fig. 12

http://www.pollution-effects.info/index_files/image029.gifRandomized trials, on the other hand, are considered to be the gold standard of study types. Here are charts provided in a 2016 randomized study dealing with breastfeeding in relation to allergies, showing results similar to many other outcomes found in the study. 

 

One could search in vain for any reference to studies negative to breastfeeding (such as those also in Section 4), or even any references to "toxins," in the Policy Statement on breastfeeding of the American Academy of Pediatrics.  Likewise there is no mention of the scores of peer-reviewed studies that have found adverse effects of breastfeeding; and nothing about the medical history of recent decades showing substantial increases in the disorders that are claimed to be reduced by breastfeeding, following the major increases that have taken place in breastfeeding.

(Full text, including references to authoritative sources, in Section 10)

 

...............................

 

  

An alternative type of infant feeding is readily available that

 

(a) contains less than 7% (and usually less than 1%) as much of the toxins discussed here, and

 

(b) was the standard feeding type for the entire U.S. generation that was born “throughout the mid-20th century,” according to the American Academy of Family Physicians.  Remember that childhood disabilities and disorders, which by now have reached high levels, were reported to have first started emerging as major chronic conditions in the 1960’s, followed by more substantial increases beginning in the 1970’s and later (see Section 1). The generation that was seldom breastfed did not have the childhood health problems that were to increase greatly after that generation was born. (Details and authoritative sources in the full version of Section 10)

 

That is something to think about, along with consideration of the increased presence of toxins in the environment and in breast milk and the considerable scientific evidence about effects of those toxins. 

 

…………………………………..

 

 

 

 

Section 1:  Substantial increases in major disorders, especially among children, beginning in the 1960’s: 

Quoting from a 2014 study in the journal Pediatrics, “Over the past half century the prevalence of childhood disability increased dramatically, coupled with notable increases in the prevalence of mental health and neurodevelopmental conditions.” (The research team whose study was just quoted had six doctoral degrees and authorship or co-authorship of 205 published studies to their credit.)4  As reported in a 2008 publication of the U.S. Center for National Health Statistics:  “Over the past three decades in the United States, behavioral and learning disorders have emerged as major chronic conditions affecting the development of school-aged children and adolescents.”5 A 2012 study by a team of scientists from the U.S., France, U.K., Denmark and New Zealand referred to the “many… major diseases – and dysfunctions – that have increased substantially in prevalence over the last 40 years;” their primary focus, regarding possible causal factors in the environment, was on the period of early development.6  In the above statements about increases in health problems, judging in each case by the report year and the number of years looking back from the report year, the period of very first emergence of major increases could be estimated to be the 1960’s, with additional and/or more noticeable increases beginning in the 1970’s.  There is substantial additional evidence in Section 10 that points to this same time of transition to declining child health.

 

The causes of the vast majority of those disorders are unknown. It is clear that their origins probably lie in environmental exposures (which include food consumed), since genetics could not change so much during such a short time span.7  It is probable that varying genetic susceptibilities influence the effects of the environmental toxins.

 

Despite the popular belief that the prenatal period is a time of far greater vulnerability to developmental toxins, development actually continues to be highly vulnerable to toxins after birth also; and exposures to developmental toxins increase greatly after birth. Evidence to support this last sentence will follow.

 

  

 

 

Section 2: 

Section 2.a:  Vulnerability of the brain’s development to toxins in the early period after birth:

 

An NIH website recognizes the early-postnatal period (along with the prenatal period) as being a time of “greatest risk” for vulnerability to developmental toxins, since “neural systems are forming before and after birth.8  A commission of the U.S. National Research Council (of the National Academies), when discussingspecific periods in development when toxicity can permanently alter the function of a system,” states that the developing brain and certain other organs may demonstrate particular sensitivity during the postnatal period.”9 Statements by the U.S. Agency for Toxic Substances and Disease Registry (ATSDR), by an international group of 24 experts, and by other academic experts also point to postnatal periods of special vulnerability to toxins.9a

 

EPA-contracted researchers in collaboration with an EPA toxicologist have stated, “postnatal exposures can impact neurodevelopment, immune function, asthma risk, reproductive development, and risk of developing metabolic disease later in life.”  Continuing, “developmental processes are, in general, most sensitive to chemical disruption if exposure occurs when the process is active.” 10 (In Figure 2 below, see major active postnatal development depicted.)  Also, according to EPA researchers, studies “have clearly demonstrated that when proliferation is actively occurring in a given region of the brain, it is vulnerable” to toxins. 11  In a publication of the National Academies Press, the authors state that “toxic exposures at a particular time would differentially affect the structures undergoing peak development.12  A publication of WHO states that “developing organs are particularly susceptible to toxic insult, given the increased rate of cell division and immaturity….”13  In the charts below, observe evidence of all of the above recognized characteristics of periods of vulnerability of the brain to toxins, all during the year after birth:  cell division and proliferation taking place (indicated by increasing cell numbers), active development (including peaks), and immaturity.

                                           

Fig. 2   (Links to sources of charts at footnote 14.)

 

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The human brain develops greatly during the first year after birth, as verified also in publications of WHO 15  and the U.S. National Research Council.16

 

According to the twelve leading U.S. scholars comprising the National Scientific Council on the Developing Child, “the time of greatest brain growth and most intensive construction of brain architecture is also the period that is most vulnerable to the relatively free passage of toxins into its cells.”16a (See the period of greatest brain growth in the left-hand chart above.) Over 30 studies have found adverse effects of postnatal exposures to toxins to be greater than effects of prenatal exposures.16b  Also note the EPA statement in Section 3.b about “the most sensitive outcome” of PBDE exposure beingadverse neurobehavioral effects following exposure during the postnatal period." This is especially significant in that levels of this serious developmental toxin in humans and in human milk increased tenfold and more during the late 20th century. (see Section 3.b)

 

Section 2.b:  Exposures to developmental toxins far greater postnatally than prenatally:

According to experts on this topic (A.A. Jensen et al.), "Significantly more (10 to 20 times) of a mother's body burden of persistent organohalogens is transferred to the infant via the milk than by the transplacental route."17  (Organohalogens include dioxins, PCBs, PBDEs, and organochlorine pesticides, all of which are neurodevelopmental toxins that are normally present in human milk.)  Two other experts on toxins involved in child development reported in 2006 that 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.139e  A 1998 German study (Drexler et al.) found that concentrations of mercury in breast milk of 85 lactating women at just two months after birth had declined by an average of over 70% from their levels at time of birth,19 and there have been compatible findings in many other studies.20  By contrast, according to what may be the only published study that compared mothers’ total mercury levels in early versus late gestation, average levels of total mercury of over a hundred women were the same at time of birth as in the third month of pregnancy.85a

 

For much more about lactation's property of concentrating environmental toxins, see the latter part of Section 4.a.2.1

 

Section 2.c:  The vulnerability to developmental toxins of concern here is to toxins to which most infants are exposed, at environmental background levels.  Quoting again from the National Scientific Council on the Developing Child:  after pointing out that “developing brain architecture is disrupted by mercury” and other neurotoxins, the Council says that the dominant source of the mercury in the U.S. that underlies this developmental disruption is coal-fired power plants, emitting mercury to the air,16a which lands in bodies of water and comes back to humans in fish and other seafood.  Not mentioned was that the mercury emissions often travel hundreds or thousands of miles before coming back to the earth’s surface. Other known neurodevelopmental toxins in the general environment are much more concentrated in urban and high-traffic areas,16c in indoor pollution,16d and in other foods, especially foods that contain animal fats. Summarizing, several toxins that are recognized to harm infant development are part of widespread background exposures of the general population, not merely isolated poisonings, as explained by the National Scientific Council on the Developing Child. (much more on this topic in Section 3)

 

It is therefore very important to look carefully at any factor that may cause those general-background exposures to become concentrated, in the process of developing infants’ becoming exposed to them.  Much of this article is devoted to just that.  One illustration is a 2006 study (Chien et al.) which determined that, of the three sources of infant mercury exposure, ingestion (breast milk), inhalation, and dermal exposure, the largest contribution was from breast milk, providing 96 to 99.6% of the total exposure.96 That is the kind of data that goes into formation of expert generalizations such as stated above in Section 2.b, indicating major concentration of toxins taking place via the process of lactation.  

  

 

The end result of infants' being exposed to toxins in concentrated form, in contrast with the reduced form that is permitted by the placental barrier, is that development is likely to be more vulnerable to toxins after birth than before. Remember that this is the relationship that has been found in over 30 studies16b and in an EPA statement about effects of the major developmental toxin, PBDEs.51

 

…………………………………

 

Section 2.d:  The early months after birth are likely to be the period most vulnerable to developmental toxins, for various reasons:

 

-- Overall growth of the brain is unusually rapid in the early weeks after birth (1% per day at first, gradually declining114h).  Remember from Section 2.a about heightened vulnerability of neurological development during rapid growth of the brain. 

--  As can be seen in Figure 2, neural connections for hearing and visual functions are forming rapidly in the first few months after birth; therefore, for any functions (such as learning ability and speech) that are dependent on processing of information received via hearing and/or vision, those early months are an especially sensitive period for effects of toxins. 

--  A report of the U.S. Public Health Service refers to the “early months after birth” as a “critical period” for development of the nervous system, during which infants are particularly vulnerable to harmful effects of toxins.93a 

--  According to an EPA report to Congress, referring to a crucial, sensitive part of organization of the brain, Neuronal migration, a process specifically affected by methylmercury,… continues until five months after birth.93

-- The U.S. Agency for Toxic Substances and Disease Registry refers to the “particularly sensitive” periods of children’s neurological development to effects of mercury, which include “the early months after birth."93b

--  Concentrations of two different developmental toxins in human milk (dioxins and mercury) have been found to be especially high during the earliest months of breastfeeding,74, 84, which is in line with long-term maternal accumulations of those toxins being excreted in the milk.85 

--  Formation of connections of the prefrontal cortex is known to take place in the first three months after birth; this development is in areas that are relevant to ASD and ADHD, including sustained attention, memory, aspects of intelligence, speech, gaze control and comprehension.  See Section 9.b for more.

 

Associations of PCB levels in early infancy with ADHD-related behaviors at age 8

 

Fig. 2a      (source of this chart:  85d)

 

image045.gifThe 2015 study that was the source of this chart was carried out by a team of researchers who are authors or coauthors of over 1700 studies among them.  Note the higher associations of childhood ADHD-related behaviors with PCB exposures when those exposures took place during early infancy, months 0 to 3; those associations of the more-exposed group, in the lower chart, are all statistically significant.  Compare those with the very minimal associations when exposures occurred after those early months.  When other researchers have failed to find effects of postnatal exposures to toxins, they were essentially always measuring exposures at times much later than the highly sensitive early months.  See the text above this chart and below here for considerable other evidence of special vulnerability during those early months.

 

 

As an indication of

(a) a possible result of this special sensitivity to toxins during the very early months after birth, together with

(b)  the increases in infants' exposures to toxins that have taken place during those early months (see Figure 7 and accompanying text),

in recent decades there have been remarkably large increases in disabilities in specific functions that undergo development during the early months after birth. (see Section 9)

 

......................................

 

 

Section 2.e:  Several studies have found associations of postnatal exposures with autism prevalence:

 

To read about four studies since 2009 that have found direct associations between autism and a distinctly postnatal exposure (breastfeeding), see Section 4; to be found among those studies are dose-response relationships as well as the observation (based on data from all 50 U.S. states and 51 U.S. counties) that "the longer the duration of exclusive breast-feeding, the greater the correlation with autism.”   Also studies will be described showing indirect associations between breastfeeding and autism, (a) in a case in which the breastfeeding-associated outcome is neurological characteristics that are known traits of autism, and (b) in the matter of pesticides, for which breastfeeding is the predominant pathway to infants, and which have been closely associated with risk of autism.

......................................

 

The rest of this article will present evidence indicating that there is one pathway for developmental toxins to infants that appears to stand out well above all other sources:  breastfeeding.  That will seem hard to believe, considering that belief in benefits of breastfeeding is so widely and strongly held.  But the evidence that points in that direction is ample and authoritative, as can be verified by checking the references that are provided with the text.

 

 

 

 

Section 3:  Developmental toxins in human milk, beginning in the mid-20th century:

 

The experts P. Grandjean and A. A. Jensen, who are authors or coauthors of 481 and 127 scientific studies, respectively, writing in the American Journal of Public Health and referring to certain environmental chemicals, pointed out in 2004 that "these substances have caused contamination of human milk only during the last half century, and long-term health impacts are now being discovered."  The specific chemicals to which they were especially referring were PCBs, dioxins, brominated flame retardants (PBDEs), and many pesticides.22

 

 

A report by the Washington State Department of Ecology discusses “Persistent Bioaccumulative Toxins,” which category includes almost all of the specific toxins to be discussed in this article:  PCBs, brominated flame retardants, dioxins, methylmercury, and pesticides.  24  In their paragraph discussing high-exposure populations, they express concern about only three groups:  people who consume fish from contaminated waters, those with exposures related to working in or residing near certain polluting industries, “and babies and young children who are breast-fed. Continuing, PBTs and metals of concern have been shown to accumulate in breast milk as a result of the mother’s exposures. (p. 64)  It is noteworthy that breastfed babies, solely because of their feeding type, are considered by the State of Washington Department of Ecology to be at the very highest level of exposure to these toxins; they share that position with only two relatively small, high-exposure groups, indicated above.

 

Note well that this discussion of breastfed babies as being at the very highest level of exposure is separate from the additional consideration of infants’ special sensitivity to toxins.

 

Later the report does bring up that second matter, pointing out that children are undergoing rapid growth and development, and therefore are particularly vulnerable to exposures that disrupt the developmental process. The only specific system whose vulnerability to toxins is mentioned in the report is the nervous system.  Special concern is expressed about formation of vital connections between the cells” of the brain; interference with this process is said to present a high risk of permanent neurobehavioral dysfunction.24  

 

Regarding the above-mentioned formation of connections between brain cells, and the risk of permanent neurological dysfunction if that process is interfered with, remember from Figure 2 and accompanying text the especially large amount of growth and formation of neural connections that normally take place during the first year after birth. 

 

So it should be noted that, according to the Washington Department of Ecology,

  (a) there is a broad group (children in general) that isparticularly vulnerable to disruptive toxins such as PCBs, PBDEs and dioxins,

  (b) within that particularly vulnerable larger group, there is a smaller subgroup (the infant age group) that has greater sensitivity; and

  (c) within that especially sensitive subgroup, a still smaller percentage is at the highest level of exposure:  breastfed infants.

 

In addition to what is stated by the above authoritative source about those who have the highest level of exposure, studies have observed that nursing infants consume a daily dioxin toxic equivalency that is 50 times that of adults.24a

 

……………………..

 

It has been authoritatively determined that typical human milk in the contemporary U.S. -- and very likely in most developed countries -- contains developmental toxins in concentrations that greatly exceed established safe levels, as follows:

 

Section 3.a:  PCBs, neurodevelopmental toxicity of which has been found in many human and animal studies, are present at high levels in human milk:

In studies published as of 2010, PCBs had been found to be present in human milk in doses 63 to 270 times the minimal risk level established by the U.S. Agency for Toxic Substances and Disease Registry.23  That report was published more than 30 years after most intentional uses of PCBs had been phased out; they are called “persistent” for good reason, and they are also present in current vehicle emissions and other sources (see text below Figure 3).  According to a 2016 study, "While banned in the 1970s, recent epidemiological data show that PCB body burdens continue to be associated with impaired reproductive and neurological health in humans." 23a  The authors cited three studies from 2009 and 2013 in support of the above statement; they also cited nine studies (six of them published between 2009 and 2015) to support their statement about "chronic effects (of PCBs) on a range of social and anxiety-related behaviors."

 

 

Early higher exposures, during the period of especially high developmental vulnerability (see Section 9) soon after birth:  The maternal body burden of one major type of PCB (153) was found in animal tests to be reduced by about 60% by lactation during the first five days of nursing.85b  See below for considerable evidence from human studies about major lactational transfers of PCBs to infants.

 

By comparison with the major transfer of PCBs by breastfeeding:  in a study by scientists with the U.S. National Institute of Environmental Health Services, who examined 104 samples of infant formula, no detectable PCBs were found in all but one sample.30

 

Section 3.a.1:  Effects of PCBs:  As one indication of effects of PCBs at common background levels, a large team of German scientists and doctors (Walkowiak et al.), 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."  25   

 

According to a 2012 review article, "a substantial body of epidemiologic literature has provided evidence that cognitive deficits are associated with elevated PCB exposures."25a

 

A 2008 American study (Stewart et al.), carried out by a team of six researchers who are authors or coauthors of over 500 published studies among them, also provided relevant results; this study was based on testing of children at the very meaningful age of 9.  (Many studies have tested children at much younger ages, before long-term effects of the toxins became apparent, and then declared that the PCBs had no detectable effects on the children.) This study's results, showing specifics about effects of relatively typical developmental PCB exposures, are indicated in the chart below:

 

Fig. 3  (Source of this chart:  See endnote 26)

 

 http://www.pollution-effects.info/index_files/image004.gif
(Note that the bottom lines are not at 0)


 

The exposures to PCBs that were linked with the cognitive declines shown in the charts above were not poisonings in the usual sense, they resulted merely from background exposures in the U.S. Great Lakes region; the exposures were to PCBs that are widely present in the environment, including from eating fish, from emissions from PCB-containing products, building materials, and other residuals from the widespread uses of earlier decades, and from various new sources, including diesel emissions, paint, cosmetics, textiles, paper, leather, printing ink, and other sources.27  The “p-values” for the first three charts just above all met the standard for statistical significance by wide margins.  The authors indicated that they found IQ deficits to be correlated with “prenatal and/or perinatal” (up to four weeks after birth) exposures of the children, which was in line with the time-of-birth time of their measurements; they made no later measurements that would have permitted correlations with exposures that occurred longer after birth.  But there are good reasons to believe that early-postnatal measurements past the perinatal period, if carried out, would have shown even greater effect than those at time of birth, as follows:

   a) postnatal exposures to such chemicals have been found to be many times greater than prenatal exposures (see Jensen quote and other text below Figure 2); also see the charts below left showing greatly increased postnatal PCB levels in breastfed children in relation to prenatal/ time-of-birth levels;

   b) after birth is a stage of development at which vulnerability to toxins continues to be high, and for some important areas of development it is a period of much greater sensitivity than during gestation (see Sections 2 and 9);

   c) as seen in the Mocarelli et al. study later, it was found in one important case that prenatal toxic exposures by themselves had no apparent effect on the child in adulthood; but prenatal exposures did affect children who were later breastfed. (The placenta serves as a protective barrier against many types of toxins; and toxins are stored in the mother’s body fat and later mobilized and transferred in concentrated form via breastfeeding).

 

Notice "freedom from distractibility" as one of the areas measured in the above charts; that is clearly something that would be relevant to a core characteristic of ADHD.  A 2015 study also found close associations between exposures to PCBs (in early infancy), at common background exposure levels, and ADHD-related behaviors;27a see Figure 2.a.

 Fig. 4

 

PCBs in relation to breastfeeding and infant formula 

Lactational transfer of PCBs to infants:  As indicated in the charts on the left,28 with corroborating evidence in Figure 5 below and in many other studies,29  exposures to PCBs after birth are likely to be far higher than before birth, especially with breastfeeding for a few months or more.

 

The steady decline of PCB levels in non-breastfed infants, shown in this chart, is compatible with

-- a) the assessment mentioned earlier in which no detectable PCBs were found in all but one of 104 samples of infant formula that were tested,30 and

-- b)  a study published in 2014, in which children at 45 months of age who had been breastfed for 6 to 12  months were found to have over 9 times the PCB concentrations compared with non-breastfed children, with even greater differences if the children had been breastfed for longer.30a This was fully compatible with another study, cited in an ATSDR report.30b

 

According to the Washington State Department of Ecology, PCBs have been shown to impact normal brain development in addition to producing other toxic effects.  PCBs have been well studied in laboratory animal and human epidemiological studies.”  Continuing, “These studies indicate that exposures to PCBs are associated with impairments in brain function resulting in deficits in IQ, memory, language and school performance.  24 (italics added)  In that same Department’s ranking of various environmental toxins for developmental effects on infants and children (Table 13, column 1), PCBs were the only toxin that joined lead in having the highest ranking for toxic effects on development. 

 

  

As published in the journal, Proceedings of the National Academy of Sciences of the United States of America, biological evidence of a link between toxins in breast milk and autism was provided in a 2007 study (Kenet et al.) carried out in the laboratory of and with guidance from M.M. Merzenich, a member of both the U.S. National Academy of Sciences and he Institute of Medicine.31  According to Dr. Merzenich, PCB intoxication was achieved by feeding the rat mother just enough of the poison to match the levels of PCB recorded in nursing human mothers in high-PCB-exposure areas of the U.S.32  Relating the results, Dr. Merzenich stated, “normal, progressive development (of the infant rats’ brains) was almost completely blocked,” about half of the rats had a “dramatically altered organization of the representations of sound frequency,” and this was of special interest because the same bizarre abnormalcies have been recorded in autistic individuals.

 

According to a summary of the above study published by the National Scientific Council on the Developing Child (which works in close collaboration with the Center on the Developing Child at Harvard University)33, the key mechanism that the brain uses for learning new skills in all animal species and humans” was found to be impaired.34

 

Dr. Merzenich pointed out that, in addition to PCBs, we should also be concerned about PBDEs, which are “close cousins” of PCBs and “very structurally similar” to the specific type of PCBs used in the experiment;35  PBDEs, like PCBs, accumulate especially in fat and breast milk.  He concluded, “If human fetal and infant effects parallel rat impacts, we would predict that there would be a correlation between the PCB/PBDE levels in human breast milk and in infant blood with the probability of autism onset.”  And there is good reason to believe that effects on human infants would parallel the effects observed in rats; animal testing is a standard way of predicting likely effects of toxins on humans -- not perfect, but good, and it is the best means of testing toxicity to humans that is available.36 

 

The study’s authors stated that, since the rat pups in the study did not have a genetic susceptibility to a developmental disorder, the vulnerability of human infants to the toxins might be greater in genetically susceptible human populations than it was in the rats.37

 

In relation to the dramatically altered representations of sound that were found to result in PCB-exposed rats in the above study, it is relevant that

-- over 77% of children with autism were reported in a survey to have hypersensitivity to particular sounds, very often causing them to try to run away from the sound;32a

-- in a study published in 2016 (Bennetto et al.), it was found that children with ASD had greatly reduced perceptions of sound in frequencies that are important to understanding speech, and the severity of autism symptoms was in proportion to the degree of hearing impairment.37c

 

With such apparent auditory distortion and/or deficits in perceptions of speech sounds in those with autism, it should not surprising that difficulties communicating are a basic characteristic of autism.  And note that PCBs, to which human infants are widely exposed (see above), were found in a controlled laboratory experiment to distort representations of sound in brains of one of our fellow mammals, after exposure at levels relevant to human environments

 

As further evidence of the relation between PCB exposure and hearing deficits, a 2014 study found an inverse association between postnatal PCB concentrations and hearing ability measured at 45-months.37d  Measures of prenatal exposure to PCBs were not associated with hearing loss. The authors pointed out that previous studies had also found

a) associations between child PCB concentrations and hearing impairment at 8-9 and at 12 years of age, and

b) no associations between prenatal PCB exposures and hearing loss.

 

To see excellent evidence that breastfeeding history is likely to  be the determinant of elevated postnatal PCB concentrations, of the kind that had the harmful effects on hearing as described above, see Figure 4 and accompanying text as well as Figure 5 just below.

 

 

PCBs exposure in relation to breastfeeding Fig. 5

 

PCBs, breastfeeding duration, and autism: 

Considering the prediction by a member of the National Academy of Sciences that is quoted above, about probability of autism in relation to PCB exposure, remember the correlations found between duration of breastfeeding and PCB levels in infants as indicated in Figure 4 above; also note this chart from the Danish Health and Medicines Authority.39   As will be seen in Section 4, several studies have found breastfeeding duration to be positively correlated with autism prevalence, including in dose-response relationships.

 

 

PCBs and learning ability:

Consider the adverse effect that distorted representations of sound (resulting from developmental PCB exposure -- see above) would be likely to have on learning ability. 

 

Also see the Colciago et al. study in Section 7.a about the strong negative effect on learning ability that has been found to result from PCB exposure, in an animal experiment.

 

 

Promoters of breastfeeding normally don’t deny the presence of toxins in human milk, but they typically seek to minimize the significance of those toxins by saying that fetuses are also exposed to the same toxins prenatally, and that the toxins are also present in infant formula. Those words are technically true in many cases, but (by ignoring the huge differences in those exposures depending on source) they also completely distort reality; this should be apparent from a review of the highly-authoritative evidence above:  Note the evidence from experts cited in Section 2.b about the many-times-greater lactational exposures to the class of toxins that includes PCBs, dioxins and PBDEs, compared with gestational exposures; and bear in mind that those greater postnatal exposures are taking place during a period of substantial vulnerability to such toxins (see Section 2), including greater vulnerability in several important areas of development. (See Section 9)  In addition, note the comparisons near the beginning of each of the subsections of Section 3 and also near the beginning of Section 8, pointing out the extreme differences between concentrations of the toxins in human milk and the concentrations in infant formula.

 

 

Effects of postnatal versus prenatal exposures to PCBs:  Among studies that have investigated effects of developmental exposure to PCBs, a thorough search by the authors of a review article (published 2009) found eight studies that fulfilled the authors’ requirements; six of those studies measured PCB levels in cord plasma and two measured PCBs in breast milk at two weeks after birth. (Those latter two studies might be considered to be one very extended study)  None of the studies that took measurements in cord plasma (which were considered to reflect prenatal exposure) found significant adverse mental effects of PCB exposure in later testing; on the other hand, the studies that measured PCB levels in breast milk did find adverse mental effects that were either fully statistically significant (in two cases) or of borderline significance (one case).38  

 

So it is noteworthy that, although PCBs are now authoritatively recognized to be neurodevelopmentally toxic, six out of six studies that looked for associations of prenatal exposures with adverse effects found no adverse effects.

 

However, the two studies in that same group that measured effects of PCBs in breast milk did find significant adverse effects. 

 

The authors pointed out that previous studies, also, had found

a) associations between child PCB concentrations and hearing impairment at 8-9 and at 12 years of age, and

b) no associations between prenatal PCB exposures and hearing loss.

  

On the same prenatal versus postnatal topic as dealt with in the above 2009 study, remember the 2014 study that found an inverse association between postnatal PCB concentrations and hearing ability measured at 45 months of age, whereas measures of prenatal exposure to PCBs were not associated with hearing loss. 37d 

 

And there have been many other studies that have also found associations of postnatal PCB exposures with adverse neurological effects, at least four of which at the same time found either no effects or only insignificant effects of prenatal exposures to PCBs.  Descriptions and citations of some of those studies have been placed in Appendix B at www.pollution-effects.info/appendixBandC.htm in order to allow moving on now to the next topics.

 

 

Section 3.a.2:  Effects of PCBs and other developmental toxins being detected well past early childhood, often only well past early childhood: 

 

 

Considering the major, widespread presence of recognized developmental toxins in human milk (other toxins will be dealt with later in this section), it may seem contradictory that doctors' associations and the U.S. CDC unreservedly promote breastfeeding except in rare cases.  When the topic of developmental toxins comes up in a web page on breastfeeding of the U.S. CDC, the document states,"despite the presence of chemical toxins (in human milk).... effects on the nursing infant have been seen only where the mother herself was clinically ill from a toxic exposure."37a  One might wonder why the CDC focuses on "effects on the nursing infant," and says nothing about later effects; there is a very large amount of evidence indicating harmful effects of infant exposures to toxins that become apparent later in childhood or life; specifically, there have been findings of delayed and long-term effects of exposures to specific toxins that are high in human milk:  PCBs, dioxins, mercury, lead, and pesticides; (information about those other toxins will be provided in later subsections of Section 3); and these long-term effects often follow exposures that produced no detectable effects during infancy. Authoritative general statements related to “long-latency delayed neurotoxicitywill be presented shortly, but first a few specific examples will be mentioned, regarding apparent effects of PCBs and other toxins that are high in human milk:

 

 

In a Michigan cohort (Jacobson et al. 1990) that was studied for effects of PCBs, developmental exposure was not related to global IQ at 4 years of age but was at age 11; similar results were obtained in another study in Oswego, New York. (Stewart et al. 2003b)38a  Remember other evidence in Section 3.a.1 indicating that adverse effects of developmental exposures to PCBs were very significant at age 9 in one case and increased with age in another study.  As described in Section 3.c. regarding the Mocarelli et al. study, lactational exposures of human males to dioxins (chemical relatives of PCBs) were found to have adverse effects on reproductive capacities as measured in adulthood; reproduction-hormonally-related effects such as found in that study would probably be unnoticed before puberty. Also in Section 3.c, note the Lee et al. study finding negative cognitive effects of background exposures to dioxins in children at ages 12 to 15.  In Figure 9, note that lower mental capacities in children at age 15 correlated well with higher average time-of-birth DDT levels according to geographic location.  The Adams and Davidson studies (in Section 3.d) both found apparent adverse effects of mercury in child populations that were in middle and late childhood. 

 

Statements by experts summarize what is known about lack of observable effects of these toxins during infancy, along with latency and major effects later, as follows:

 

EPA scientists refer to “long-latency delayed neurotoxicity” when discussing effects of methylmercury and also of a component of various pesticides.38e  The  ATSDR (U.S. Agency for Toxic Substances and Disease Registry) states, referring to detection of effects of lead on the developing nervous system during early childhood,  "it is often impossible to determine these effects upon clinical examination."38h  The neurology expert, Bernard Weiss, discussing effects of developmental exposure to environmental toxins, says that often “manifestations of damage emerge only after compensatory processes have been exhausted…. Latency periods as long as 15 years have been reported...." (following methylmercury exposure)38f  According to a publication of WHO, “Many diseases that are caused by toxicants in the environment require decades to develop." (Specific toxicants causing the diseases discussed were said to be lead, mercury, and endocrine disruptors; the latter category includes PCBs and dioxins.)  Continuing  on the subject of diseases caused by toxicants, "Many such diseases, including cancer and neurodegenerative diseases, are now thought to arise through a series of stages that require years or even decades from initiation to actual manifestation of disease.”38g A commission of the U.S. National Academy of Sciences says essentially the same thing about latencies with regard to effects of pesticides.38n

 

Regarding long-latency effects of developmental lead exposure, the ATSDR points out that "childhood lead poisoning can lead to health effects later in life...."38h (See later in Section 3.e about the substantial lead content that is widely present in human milk, compared with none found in infant formula in the U.S. in recent years.)

.  

Animal experiments provide confirmation of the human studies, regarding increased effects with age.  In a 2006 Swedish study, neurological defects that resulted from developmental exposure to PCBs and PBDEs worsened with age;38m the brain PCB concentrations produced in the experiment were in the same order of magnitude as has been found in human infants and were administered at the equivalent of human time of birth,38c and the effects included defects in learning ability and memory in adulthood.  In a 2007 study, peri-natal exposures to PCBs (as well as methylmercury) were found to greatly reduce certain brain components that are important to higher cognitive function, but only in measurements taken as of the rat age that was equivalent to human age 17; such damage was not observed in the assessments of rats at younger ages, including at puberty.38b, 38c  An animal experiment (Kaya et al.) will be described in Section 7.b.2  in which the effect of developmental exposure to PCBs in reducing testosterone was nearly three times as great in adulthood as it had been in infancy; bear in mind that testosterone is important to male mental functioning -- see early in Section 7.bAlso see the Colciago et al. study in Section 7.a about the strong effect on learning ability in adult rats that has been found to result from developmental PCB exposure, in an animal experiment.

 

Also, the several studies (in Section 4) that found positive correlations between breastfeeding rates and autism prevalence are relevant to a discussion of long-term effects of developmental exposures to toxins, since autism prevalence statistics are normally determined in relation to children age 8 and older.  That is apparently due to autism often not being diagnosed until age 8 and later.

 

To return briefly to the CDC statement that prompted the above discussion of long-term effects of exposures to toxins during infancy, that statement will be repeated here:  The CDC document says,"despite the presence of chemical toxins (in human milk).... effects on the nursing infant have been seen only where the mother herself was clinically ill from a toxic exposure."37a  Given the substantial evidence in the previous 5-6 paragraphs about long-term effects of exposures during infancy to toxins that are undisputedly high in human milk, including effects that are often observed only after years or decades, one may wonder why anybody would bother to discuss what is apparent only during infancy.  

 

 

The American Academy of Pediatrics, despite the very ample evidence of developmental toxins in average human milk (see earlier and later in Section 3), does not mention environmental toxins even once in its policy statement, "Breastfeeding and the Use of Human Milk."37b  One might wonder whether the phrase, "the whole truth," has any meaning to some people when they are comfortably sitting on a bandwagon.  Such telling of half-truths would be excusable if parents were generally aware of the important information that is being withheld, but that is certainly not the case here.

 

Section 3.a.3:  Various studies have failed to find adverse effects of the developmental toxins in human milk when testing children in early childhood; and promoters of breastfeeding point to those studies as evidence of lack of harmful effects of those toxins.  Considering the contents of Section 3.a.2 (just above), one may wonder whether it is sensible to say something about failure to find adverse effects in early childhood as if that is all that matters, while saying nothing about the negative long-term effects.

 

 

Section 3.b:  Brominated flame retardants, EPA-recognized neurodevelopmental toxins to which sensitivity is greatest postnatally:

 

Of the two principal types of brominated flame retardants, PBDEs are more thoroughly studied, but HBCDs are also recognized to have substantial adverse effects.

 

HBCDs and their adverse effects: The EPA has assigned to HBCDs a “High hazard” designation (its highest designation) for developmental neurotoxicity, as well as other levels of hazard for its other toxic effects.40 

 

HBCD ingestion by breastfed infants has been found to be seventeen times as high as HBCD ingestion by formula-fed infants. (All of the detectable HBCD ingested by the formula-fed infants came from drinking water.)73

 

For more information about this toxin, see “High and increasing levels of HBCDs in human milk” later.

 

Adverse effects of PBDEs:  According to the U.S. Agency for Toxic Substances and Disease Registry, results from human studies are suggestive of an effect of PBDEs on neurodevelopment in children, including impaired cognitive development (comprehension, memory), impaired motor skills, increased impulsivity, and decreased attention.42  Whereas the ATSDR indicates probability above, an EPA statement (a few paragraphs down) indicates nothing but certainty regarding adverse neurobehavioral effects” of PBDEs, following postnatal exposures;(a) and the EPA clearly sees those effects as being serious; they refer to neurobehavioral effects of PBDE exposures as being a “critical endpoint of concern.”43  As reported in a 2014 review of studies, ““the majority of the epidemiologic evidence supports that early life exposure to PBDEs measured during pregnancy and/or during childhood is detrimental to child neurodevelopment in domains related to child behavior, cognition, and motor skills.”43b  A 2015 European Union study by a panel of experts estimated about 3300 cases of intellectual disability annually, plus significant losses of IQ in the general population, as a result of exposures to PBDEs in the EU.43c

 

According to early data, concentrations of PBDEs in infant formula were found to be at levels less than 3% as high as in average U.S. breast milk.55 But according to more recent data that applies to the specific type of PBDE (BDE 209) that has been by far the most widespread type in recent years, that chemical has been found to be one eight-hundredth to one nine-thousandth as high in infant formula as in human milk.56

 

Adverse effects of brominated flame retardants in general, especially related to ADHD, have been observed; also found have been worse fine manipulative abilities.56a  See also two of the studies at "Effects of exposures..." next to/below Figure 5a for other evidence about associations with ADHD-related behavior.

 

image043.gifFig. 5.1

High, ongoing exposures to PBDEs, including infant exposures:

 

PBDE levels were doubling in humans approximately every three to five years during the later decades leading up to the 2000's.114d  According to a 2007 report to the Maine legislature by an official of the Maine CDC, ”Several studies reported that levels of PBDEs in human tissues are now higher than PCBs, including in the U.S.;” in two out of 52 individuals in one study, PBDE levels were found to be 100 times greater than PCBs.114d 

 

To put the above in perspective, remember the data presented earlier (in a 2010 report from the Oregon Department of Environmental Quality) stating that PCBs have been found to be present in human milk in doses 63 to 270 times the minimal risk level established by the U.S. Agency for Toxic Substances and Disease Registry.” 23  Going by the above, together with Dr. Merzenich’s statement of the similarities of the two chemicals, it appears that half of American breastfed infants in 2007 had exposures to PBDEs that were as bad as, and sometimes even worse than, their already-high exposures to PCBs.  

 

In a 2007 study of Spanish children, it was found that PBDEs were about five times higher in 4-year-old children who had been breastfed than in 4-year-olds who had been formula fed.54

 

An EPA web page on PBDEs,50 accessed in January of 2016, pointed out that “despite the United States having phased out the manufacture and import of (two types of PBDEs) in 2004, their component congeners are being detected in humans and the environment. Some reports indicate that levels are increasing.”  The EPA mentions nothing about any reports of declining levels of PBDEs; but it does refer to the chemical’s persistence (including in relation to continued use of furnishings and electronics containing them, and their presence in waste sites), and their presence in imported products.  In addition, PBDEs are also components of combustion emissions, including from power plants and vehicles,44 especially diesel-powered vehicles,45 46 and those emissions are continuing.  For other studies providing additional evidence regarding the ongoing high human exposures to PBDEs, especially from combustion sources and in urban air, the extremes of exposures of breastfed children to PBDEs, and effects of PBDEs in reducing levels of the neurodevelopmentally-important testosterone, see Appendix C.

 

Given the ongoing, high infant exposures to PBDEs via breastfeeding, the following statement by the U.S. EPA about PBDEs has special significance:

“The most sensitive outcome of PBDE exposure is adverse neurobehavioral effects following exposure during the postnatal period."51

 

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High and increasing levels of HBCDs in human milk:

 

In a 2010 U.K. study, HBCDs were found in every sample of human milk examined in the study, and average daily exposure of an infant to HBCDs via breast milk alone was found to be four times higher than the average adult’s combined exposures (per pound of body weight) from diet, inhalation and dust ingestion. In addition, infants at the 95th percentile had exposure over three times higher than that average exposure.41

 

Knowing the above, remember that the EPA has assigned to HBCDs a "High hazard" designation (its highest level) for developmental neurotoxicity, as well as other levels of hazard for its other toxic effects.40  It is also relevant that the EPA has determined that exposure to the other principal brominated flame retardant, PBDEs, has its “most sensitive outcome following exposure during the postnatal period.51

 

increase in flame retardants in breast milk Fig. 5a

In an article that drew data on brominated flame retardants in Europe and Asia from over 100 studies published in 2005-2007, the researchers concluded that “Generally, trends show a levelling in concentrations of BDEs and increases in concentrations of HBCD wherever determined.”48  (Note that HBCD is the same as the HBCDD referred to in this chart.)  A 2008 French study found that “concentration levels (of HBCDs) measured in quantifiable breast milk samples were around 10 to 100 times higher than the levels usually observed for other organic pollutants.65  A study of pollutants in human milk in Belgium compared levels in 2009-2010 with levels in a previous study in 2006 and found that the concentrations of most pollutants in the more recent study were lower or comparable to the concentrations in the 2006 study, but levels of HBCD in human milk increased by 153% during that relatively brief period.66

 

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Effects of exposures even at relatively low levels:

Levels of PBDEs outside the U.S. have been found to be one-tenth to one-hundredth as high as in the U.S. (They have been high in the U.S. due to California law which, for decades before 2015, required use of flame retardants in cushioning and electronics.)  But even the relatively minor exposures outside the U.S. appear to have been having adverse effects.  Two Spanish studies and a Taiwanese study found as follows:

   a) Gestational exposure to PBDEs had no significant adverse effect on 4-year-olds, but exposure to those same mothers' PBDE levels via breastfeeding did have a substantial effect, including an 80% increase in relative risk of attention-deficit problems and a 160% increased relative risk of poor social competence.57 (Note that “poor social competence” is a way of describing a basic characteristic of people with autism.)

    b)  Researchers found “an association between PBDE concentrations in colostrum (early breast milk) and impaired infant cognitive development."  The authors also pointed out that “in the group of children breastfed for a longer period the association between BDE-209 exposure and neuro-development impairment was somewhat stronger….  Further, associations in the longer breastfeeding group may be underestimated…"(going on to explain the reason for that).58  

     c)  According to a study by four Taiwanese scientists, Neonatal (relating to infants in the first month after birth) BDE-209 exposure has been demonstrated to have neurotoxic effects in most in vivo studies.”  Continuing, “Neonatal exposure to BDE-209 has been found to have developmental neurotoxicity, including hyperactivity; learning and memory defects; a reduction in habituation;….59  It should be noted that exposures of infants to this chemical would have been predominantly a result of transfers via breastfeeding; remember the 2007 study’s finding that PBDEs were about five times higher in 4-year-old children who had been breastfed than in 4-year-olds who had been formula fed.54

 

None of the above three studies showed results broken down according to narrowly-segmented levels of exposure.58a  Narrowly-segmented breakdowns might well reveal far more serious effects at the highest exposure levels, since a U.S. study (Schecter et al.) found that PBDE levels in the top 5% of the population were 10 to 100 times the median levels;60 in a Chinese study, children at the 95th percentile were found to have levels over 12 times the median level.61  Consider how much greater the neurodevelopmental effects could be of the many-times-higher exposures in the top few percentiles, compared with the already substantial differences found in the above studies in which the most-exposed measured group was made up of a third or more of the population studied.

 

 

More about effects of PBDEs (specifically related to reduction of male hormones and therefore to neurological development) will be presented later, in Section 7

 

Sources of exposure to HBCD (HBCDD)

HBCDs, also, are used as flame retardants, in construction materials and in home goods.  They have been found in human milk and serum throughout the world, although they have received comparatively little attention in the United States.63  A 2012 U.S. study (Carignan et al.) found HBCD in all samples of breast milk tested, with a 39% increase in milk HBCD levels linked with a mother’s residence in a carpeted home, a 17% increase in milk HBCD per item of stereo or video electronics in the home, and a substantial decrease in milk of mothers who regularly chose organic foods.64

 

One noteworthy characteristic of HBCD exposure is the extremes of exposures within the general population. An American study, testing HBCD levels in dust of 19 Boston-area homes, found that the exposures varied by a ratio of 29,000 to 1;67 and a U.K. study found high-end exposure to HBCDs in house dust that was also about that high.68  Those high levels of HBCD in dust almost certainly heavily affect HBCD levels in mothers’ milk; remember from just above the close associations that were found between HBCDs in a mother’s milk and presence in the woman’s home of electronics and carpeting. In a 2008 U.S. study, house dust accounted for over 80% of estimated human intake of PBDEs (the other, more studied, brominated flame retardant);69  other studies have arrived at compatible findings,70 including with HBCDs.71  

 

All of the above strongly imply that, with household HBCD dust levels found to vary by a ratio of 29,000 to 1 even within a study group of only 19 households, some of the breast milk concentrations of this chemical that is designated by the EPA to be a “high hazard” for developmental neurotoxicity40 could probably harm the development of a significant number of infants.

 

Remember from Figures 5.1 and 5.a and accompanying text the high and long- growing levels of PBDEs and HBCDs in humans and in breast milk, with “increases in concentrations of HBCD wherever determined,” as indicated in studies published in 2005-2007.

 

Also bear in mind the following:

-- experts have stated (as quoted earlier) that "Significantly more (10 to 20 times) of a mother's body burden of persistent organohalogens (which includes HBCDs and PBDEs) is transferred to the infant via the milk than by the transplacental route,"17 and

 -- breastfed infants were found to receive 17 times as much HBCD as formula-fed infants (see beginning of Section 3.b).

 

 

Section 3.c:  Dioxins, with long-term harmful effects found at advanced ages; breastfeeding found to have been the main determinant of long-term dioxin levels:

 

Dioxins are part of the same chemical family (organohalogens) of which PCBs, PBDEs and HBCDs are members.  Remember the expert statement just above indicating extremely high transfer of this class of chemicals to infants via breast milk.17  Even though levels of dioxins in breast milk in a number of countries have been declining since about the 1960’s, dioxin has still been found to be present in breast milk in concentrations scores to hundreds of times higher than the relatively safe reference dose (RfD) established by the EPA, as found in studies from many countries carried out during the 2000’s.73a  Dioxin has been found to be present in breast milk at over 100 times the concentration in infant formula.75

 

Early higher exposures, during the period of especially high developmental vulnerability (see Section 9) soon after birth:  Concentrations in breast milk initially after birth in the U.S. appear to be typically hundreds of times the EPA’s reference dose, tapering off to 20 or so times the RfD over the course of a year of breastfeeding.74  

 

A major toxicology textbook published in 2011, with 21 contributing authors, states as follows regarding dioxins (as well as PCBs):  “These studies have indicated that … the most susceptible period of exposure is during development and nursing.” Also, “early developmental exposures to these chemicals are particularly devastating.” (p. 551, bottom)131

One effect of dioxins, which has been verified in animal experiments, is reduction of testosterone production in males.  This would be expected to have an effect on human reproduction, which is a significant concern at a time when most developed countries have declining populations, leading to concerns about viability of social security systems; those declines are occurring despite major expenditures on artificial reproductive technologies, with accompanying health risks.  But testosterone is also important to neurological development.  More about neurological effects of dioxins, especially on males (who are disproportionately affected by autism, ADHD and other neurological disorders), will come in Section 7.

 

The effect of reducing male hormones was illustrated in the case of accidental exposures in Seveso, Italy.  A 2011 study (by Mocarelli and 12 others)76  of the aftermath of that accident measured characteristics of sons of mothers who had been exposed to increased levels of dioxins before their sons’ births, resulting in what the authors called “modest elevations” of the mothers’ dioxin levels.  When the sons’ sperm quality and hormone concentrations were examined at ages 18 to 26, those who had been breastfed (and only those who had been breastfed) showed seriously adverse effects in all of the four different reproduction-related areas that were measured; by contrast, those who had been formula-fed showed no effects.  It should also be mentioned that, at those late ages, average dioxin concentrations were still twice as high in the breastfed young men as in those who had been formula fed, in both the exposed group and in the comparison group.77

 

The high levels of dioxins in breastfed young men, even decades after infancy, is explainable partly by the known persistence of these chemicals in the body and partly by the extremes of exposure via breastfeeding. In the above Mocarelli study, it was determined that the median levels of dioxins in breastfed infants were doubled within 4-5 months after birth, compared with levels in formula-fed infants that were reduced by half in that same period of time.76  A German study found that, at 11 months of age, dioxin toxicity-equivalent concentrations in breastfed infants had become about 10 times higher than in formula-fed infants.79

 

To aid in understanding why prenatal exposures should have had effects on breastfed but not on formula-fed children, bear in mind that

  (a) the “placental barrier” has that name for a reason (more so in relation to some toxins than others); the placenta probably provides some protection to the fetus from dioxins during gestation; and

  (b) dioxins (like many other toxins) accumulate in the body, are stored in maternal fat, and are later mobilized and excreted in greatly concentrated form in breast milk.  (see Jensen quote and accompanying text below Figure 2)

 

Another illustration of effects of dioxins was found in a 2007 study by an international research team (Lee et al.) that tested children at ages 12 and 15, thereby permitting good indications of long-term effects of developmental toxins. This study found that learning disability and attention deficit disorder were two and three times as high among children with elevated levels of dioxins, compared with children with undetectable dioxin levels.80  The dioxins associated with such dramatic increases in risk of neurological disorders were at common levels -- found in 27% to 31% of children. Remember from the Mocarelli study above that breastfeeding is by far the main determinant of dioxin levels even far past infancy.

 

Section 3.d:  Mercury is often already high at birth, then a mother’s long-term accumulations are rapidly transferred in breast milk; “clearly documented toxic effects on the immature brain” occur during the postnatal period.

 

Mercury is the fourth developmental toxin that is normally present in human milk at levels greatly exceeding established safe doses.  Breast milk typically has mercury concentrations that are about eight times the WHO guideline for drinking-water quality81 and four times the concentration that is allowed in U.S. bottled water,82 and often higher. And mercury in infant formula has been found to be less than 1% as high as in human milk.83

 

Ethylmercury, as has often been used in vaccines, has been widely vindicated as having a role in contributing to autism.  But ethylmercury is only one of a number of species of mercury, and several other forms are authoritatively recognized to be neurological toxins. Methylmercury is listed by the International Program of Chemical Safety as one of the six most dangerous chemicals in the world's environment.83a  Data from a major U.S. government survey indicates that methylmercury comprises about  82% to 94% of the mercury in women whose mercury levels are in the top quarter.92

 

Early higher exposures, during the period of especially high developmental vulnerability (see Section 9) soon after birth:  A 1998 German study (Drexler et al.) 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;84 and there have been compatible findings in many other studies.85  In a Saudi study, the number of children a mother had breastfed was found to have a highly-significant negative effect on the mercury level in her breast milk, indicating substantial transfers of long-term accumulations of mercury to earlier infants.85c

 

Many studies related to mercury, such as those indicated above, illustrate the tendency of the toxins to accumulate in women’s bodies over the years and to be rapidly transferred to infants in concentrated form during lactation.  The transfer of so much of a mother’s accumulations of mercury to a breastfed infant is apparently rather sudden, from a supply that has not been significantly reduced during gestation; according to what may be the only study that compared mothers’ total mercury levels in early versus late gestation, average levels of total mercury of over a hundred women were the same at gestational week 37 as at gestational week 12.85a 

 

In a study by a highly-published scientist (P. Grandjean) and his team, it was found that total mercury concentrations in infants that had been breastfed for one year were three times as high as those in infants that had not been breastfed.100  Another study found more than doubling of infant mercury levels due to 6 months of breastfeeding.101  The mean mercury concentration in the hair of breastfed Spanish babies was found to be about 1.5 times higher than that found in their mother's hair, with a highly significant correlation.101a

 

In relation to those blood mercury figures, it is relevant that levels of methylmercury in the human brain are approximately six times higher than blood mercury levels.83a

 

The rapid transfer of much of a fully-grown person’s long-term accumulations of neurodevelopmental toxins to a small infant occurs at a time of overall high vulnerability of the infant, due to the active neurological development taking place at the same time as breastfeeding (see Figure 2 and accompanying text). But there is also specific extra vulnerability for a large fraction of the infant population; in a 2011 study reporting research by health departments of three U.S. states, it was found that about 8% of infants at birth already have mercury levels exceeding the EPA’s relatively-safe Reference Dose;86 similar levels, affecting over 300,000 infants per year in the U.S. alone, were found in a national survey.87

 

That is over a quarter-million U.S. infants per year who have mercury levels above the established safe level even before the substantial transfers that will usually take place via breastfeeding.

 

A publication of Harvard University’s Center on the Developing Child, when discussing “prenatal and early childhood exposures to substances that have clearly documented toxic effects on the immature brain,” mentions only three leading examples of such well-documented neurodevelopmental toxins, one of which is mercury.88  The authors gave mercury in fish as a specific example of a source of toxins of concern, indicating that exposures expected to cause neurological harm can consist merely of relatively normal dietary exposures.

 

Related to the above authoritative statement about early childhood exposures (including mercury via food) having “toxic effects on the immature brain:  observe the fundamentally immature state of the brain in the first year after birth, as illustrated in Figure 2 earlier.

 

A 2013 study (Adams et al.), by a team of 12 researchers  investigating children age 5 to 16, found that mercury stood out from among various metals that were studied for their associations with autism.  Levels of several metals including mercury were found to be associated with autism and were also “strongly associated with variations in the severity of autism.”  But mercury was the variable that was “most consistently significant” in relation to increased autism in both red blood cells and whole blood. 89 The p-value for that relationship was .0003, meaning there were only three chances out of 10,000 that the finding regarding autism-related effects of mercury was a random occurrence.  A dose-response association such as this (severity of outcomes varying in relation to measured levels of toxins) is considered to be good evidence of a causal relationship.

  

Knowing about methylmercury’s importance among mercury forms in human blood, 92 note that, according to the EPA, “There is general agreement that the nervous system continues development in post-natal life and that methylmercury can adversely affect the developmental processes.” 90  According to a publication of WHO, Methylmercury is highly toxic, particularly to the nervous system; the developing brain is thought to be the most sensitive target organ for toxicity.90a See Figure 2 and accompanying text for indication of how much development of the brain takes place during the year after birth.

  

According to an EPA report to Congress, referring to a crucial part of organization of the brain, Neuronal migration, a process specifically affected by methylmercury,… continues until five months after birth.93 (italics added)  Note that those five months of recognized special vulnerability of a critical part of brain formation occur during a period of major exposure of infants to mercury, as that toxin is transferred from mothers by breastfeeding:  remember Drexler et al. and related studies regarding rapid excretion of much of a grown woman’s long-term accumulation of mercury in breast milk during the first months after birth; also note the Chien et al. study below about the extreme dominance of breastfeeding as a source of mercury to infants.  And remember that these transfers take place to newborns many of whom start out with mercury levels already exceeding the EPA’s Reference Dose.86, 87

 

 

At least ten published studies have found high levels of mercury in those with ASD (autism spectrum disorders).94 A 2007 study determined the levels of mercury, lead, and zinc in baby teeth of children with autism spectrum disorder and found that children with autism had significantly (2.1-fold) higher levels of mercury in their baby teeth, but similar levels of lead and zinc.95  As the authors pointed out, baby teeth are a good measure of cumulative exposure to metals that occurred during early infancy. Remember the dose-response relationship between mercury levels and variations in severity of autism found in the Adams et al. study described earlier in this section.  For several other studies finding associations between mercury and autism, see Section 3.e.2.h

 

Bearing in mind the above very substantial evidence linking autism with exposure to mercury, especially with exposures occurring during early infancy, note in the Chien study just below how dominant breast milk can be as a source of mercury to infants, and remember that mercury in infant formula has been found to be less than 1% as high as in human milk.83

 

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

 

The extremely low proportion of mercury taken in by inhalation (compared with via breast milk) as reported just above should be borne in mind when reading the following:  A study in the San Francisco Bay area found that atmospheric exposures to metals, especially mercury, were associated with autism prevalence.97  It would seem reasonable to suggest that, with such a small percentage of an infant’s intake of mercury being via inhalation (as found in the Chien study), the autism-linked effects of the atmospheric mercury found in the above study probably would have been by way of the mothers who had been inhaling that air for years, into adult-size lungs, followed by rapid transfer of the accumulated mercury to an infant.  Lactational transfer comes at a time of high developmental vulnerability, as explained earlier (Section 2) and as indicated in the EPA statement about vulnerability of neuronal migration to effects of mercury for several months after birth.  

Fig. 6

 

Effects of mercury toxin on development of boysAdverse effects of mercury (as well as of the other toxins described earlier) are not limited to diagnosed disorders.  This chart (from Davidson et al., 2010)98 shows effects observed in a general population of students in a study carried out in the Seychelles, showing apparent effects on scholastic achievement from moderately elevated mercury levels due to fish consumption. 

 

Both autism and ADHD, as well as some other neurological disorders, are known to predominantly affect males,99 in a ratio of almost 5 to 1 in the case of autism, for unknown reasons.  Therefore it is significant to see evidence (in this set of charts) of widespread, adverse cognitive effects -- primarily on males -- associated with variations in postnatal levels of mercury.  For much more about greater effects of various developmental toxins (including mercury) on males than on females, see Section 7.

 

 

For much more on developmental effects of mercury, see www.mercury-effects.info.

 

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Section 3.e:  Pesticides and lead: 

The four toxins discussed above are the four that are contained in breast milk in concentrations known to far exceed established relatively safe levels. But there are two additional important toxins contained in breast milk about which there is also substantial evidence indicating harmful developmental effects, even though there are no established thresholds that permit comparisons with safe levels in these cases.

Section 3.e.1:  For information about pesticides, their known harmful neurodevelopmental effects, their substantial presence in human milk, and their absence in infant formula in the U.S., see Section 8.

 

Section 3.e.2:  Lead:

The EPA web page on lead, accessed in June of 2016, re-states its long-standing position that harmful effects of lead "may occur at blood lead levels so low as to be essentially without a threshold." 98a The CDC and the American Academy of Pediatrics concur with this position.98e  According to a 2014 article in the American Journal of Public Health, "research has continually shown that no amount of lead exposure is safe," citing seven studies in support of that statement.98e1  

 

It will be explained in this section that lead is transferred to infants in breast milk, and it is transferred in doses high enough to significantly increase risk of neurodevelopmental harm.  But before that, it should be pointed out that a U.S. Food and Drug Administration study for the period 2006-2011 tested 34 samples of milk-based infant formula and found no detectable lead in any of the samples.98b  In an earlier FDA test, only one sample out of 88 contained any measurable lead, and that one was at a concentration (0.007 mg/kg, = 7mcg/kg = approx. 0.7 mcg/dL)98b that is considered to be acceptable in breast milk.  (These results were low compared with what had been found in earlier decades, before use of lead solder in cans was discontinued.)

Fig. 6.0

leadBF.gifAs calculated in a 2004 study98d (see chart on right), lead in breast milk accounted for 12% of the variance in infant blood lead levels after only one month of breastfeeding.  In a subsequent study, this time using a breastfeeding period of three months, a 1 mcg increase in maternal blood lead was found to be associated with an increase in infant lead levels several times the assessment at one month.98d3  A 1998 study's calculations indicated that "from 36 to 80% of lead in blood in the first 60-90 days postpartum is contributed from breast milk."98d2  A 2001 study estimated the contribution of breastfeeding to three infants' blood lead levels to be 40%, 60%, and  65%, based on 58 to 66 days of breastfeeding.98d1 

 

The above findings are compatible with the known effect of breastfeeding in increasing infant blood levels, as reported by the U.S. CDC.  A 2010 CDC publication includes a chart showing ten different possible breast milk lead levels across a wide range of likely concentrations; it is noteworthy that at every lead level shown, including the lowest (1 mcg/dL), breastfeeding is shown to always result in an increase in infant blood lead concentrations.98g1  Note in Figure 6.0a and accompanying text and in studies referenced there and in Section 3.e.2.d that women's blood levels increase greatly during lactation and would normally be well above that 1 mcg/dL level during lactation.  The increases in infant  lead levels may be small with each individual feeding of breast milk; but many small amounts can add up to significant totals, especially considering that (a) lead is known to accumulate in the body,98g and (b) according to the EPA, harmful effects of lead "may occur at blood lead levels so low as to be essentially without a threshold." 98a

 

So (going back two paragraphs) breastfeeding has been found to be likely to be the predominant source of an infant's lead levels even after less than three months of breastfeeding; that was a normal time range for  breastfeeding duration in the 1990's, when the above studies were carried out.  Typical breastfeeding in current years in the U.S. and most European countries would be likely to be of longer duration than that, on average, and would also be more likely to be exclusive (see Figures 7 and 8.a and CDC document at 98f1).

  

Bear in mind the 2016 policy statement on lead toxicity of the American Academy of Pediatrics, in which it says (in line with the EPA's position98a), "it is now recognized that there is no safe level of lead exposure," and "all sources of lead exposure should be eliminated." 98g (emphasis added)   The U.S. ATSDR holds that same position, saying "It is important to prevent all lead exposures."38h

  

Promoters of breastfeeding point out that concentrations of lead in breast milk are far lower than in maternal blood; the intended implication is that transfer of lead via breastfeeding is therefore not very significant.  But that would be a false impression to convey, since lead accumulates in the body.98g  Clearly, what matters is the total lead that ends up within the infant.  And that can turn out to be very significant even though it is received in small doses, if the doses are numerous. (See Figure 6.0 above and accompanying text about how substantially transfers of lead via breastfeeding can contribute to an infant's lead levels.) There is excellent evidence linking lead, including in the concentrations that are found in many tens of thousands of infants in the contemporary U.S., with greater risk of both autism (see Section 3.2.e.h) and ADHD (see Section 3.e.2.i) later.

 

Remember from above the CDC's estimates that breastfeeding would always result in an increase in infant blood lead concentrations, even at the lowest levels of maternal lead that the CDC considers it to be appropriate to report about.  And bear in mind that infant formula in the U.S. has been found to contain essentially no lead. 98b

 

Soil and dust are sources of child exposure to lead in addition to food, after early infancy; but in the early months after birth, those are considered to be of little relevance. 98g2  Infants would not yet be at the stage of normal hand-to-mouth activity until 6 months after birth,98g6 which would be past the especially vulnerable early months after birth. (see Sections 2.d and 9)

  

Given the above, and considering the position of the AAP and the EPA that "there is no safe level of lead exposure," and bearing in mind the other toxins known to be present in human milk in concentrations exceeding established safe levels (see earlier in Section 3), one would expect any recommendation of breastfeeding to be based only on a cautious, thorough consideration of all evidence.  For good reasons, it is normal in modern times for important decisions on medical and scientific matters to be based on a written analysis of all significant evidence.  But, when the American Academy of Pediatrics and the American Academy of Family Physicians are repeatedly asked how they decided to promote breastfeeding despite the recognized presence of toxins in human milk at authoritatively-recognized hazardous levels, they never respond.  If such a decision had been made properly, following due consideration of the appropriate negative as well as positive evidence, a written record of the basis for the decision would be sitting in the file and ready to be sent out on request. Better yet, it should be published.  But that is clearly not the case here, strongly implying that there has been no judgment based on careful review of all evidence, in this matter.

 .

....................................

 

To summarize some key points from above: 

 

-- lead is known to accumulate in the body even though it is received in very small doses;

 

-- U.S. infant formula of recent years has been authoritatively found to contain no detectable lead;

 

-- human milk does contain lead (although in greatly varying concentrations);

 

-- lead received via breastfeeding, especially with more than two months of nursing, is likely to constitute most of the lead in an infant, at the developmentally most vulnerable time of the child's life;

 

-- according to eminently authoritative sources, with no apparent disagreement, "...it is now recognized that there is no safe level of lead exposure;"

 

As will be described in laler subsections, there is also substantial evidence in numerous studies linking lead, in concentrations that are found in many tens of thousands of infants in the contemporary U.S., with greater risk of autism (see Sections 3.e.2.g- 3.e.2.h) and ADHD (see Section 3.e.2.i).

 

 

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3.e.2.a:  Sources of lead in women, and therefore in breast milk, include occupational and hobby exposures, cosmetics, common foods, local and regional industrial pollution, and many other sources:

 

   a) occupational and hobby exposures of the mothers and of household members who bring home deposited dust:   exposures occur in manufacturing of ceramics, glass and plastics, and home renovation, pottery making, jewelry making, use of dyes, and many other categories; 98b, 98u, 98i in a Chinese study, lead in breast milk was found to be almost 12 times as high in occupationally lead-exposed women as in occupationally non-exposed women.98f

   b) Cosmetics:  Traditional eyeliners popular in many parts of the world are high in lead, and have been linked with lead poisoning;98j,.98p The U.S. Food and Drug Administration had a survey done in 2010 analyzing lead contents of 400 different lipsticks purchased in retail stores, in which lead was found in all lipstick samples tested; 11 of them, mostly brand-name products, had lead contents of over 4000 parts per billion;98c for comparison, the EPA's action level for lead in drinking water is 15 parts per billion;98v bear in mind that (a) lipstick is applied (often many times a day, every day) at a location where it can easily rub off and enter the body in connection with eating and lip licking, and (b) lead is known to the U.S. ATSDR to be absorbed through the skin as well as by inhalation,98h both of which would be relevant to lipstick; also (c) lead accumulates in the body, over decades (more on this below).

   c) according to the U.S. FDA, a child-bearing woman's diet contributes an average of 43% of her lead levels;98k the FDA says that "many food products would be expected to contain very small amounts" of lead; the FDA has found lead in juices, fruit, carrots, sweet potatoes, candy, and other common foods.98u1 A Polish study found lead present in vegetables in general, especially in potatoes, grains and cereals.98u2  Apparently those "very small amounts" add up over the years.

   d) Other common sources are industrial and cottage industry emissions (which are especially high in developing countries),98u urban pollution (including in developed countries),98r use of traditional lead-glazed pottery, eating of non-food substances (pica -- which is common in Africa, Latin America, and U.S. immigrant communities), culturally-specific practices (such as use of lead-containing alternative remedies),98x leaded paint and leaded gasoline exhaust in the many countries in which those are still legal or only recently banned; and residence in older housing even in developed countries.  Leaded fuel is still used in piston-engine aircraft, of which there are currently over 150,000 in the U.S., and over 16 million Americans live within a kilometer of airports used by such aircraft.  Several hundred thousand tons of lead are emitted into the air annually by industrial processes and electric generation in the U.S., as of 2008 data. 98t (According to the U.S. ATSDR,  "almost all inhaled lead is absorbed into the body."98h)  In a town with industrial pollution, lead concentrations in breast milk were found to be 420 parts per billion, compared with 30 ppb in the control group.98w

 

Remember from above that the FDA, in its most recent test, found no detectable lead in scores of samples of infant formula.  Cows and their milk benefit from much less exposure to the many lead sources indicated above as well as from continuous clearing of toxins out of cows' bodies via regular milking.

 

 

3.e.2.c:  Effects of lead, even at very low doses, are well known, but to quote the U.S. CDC for a brief summary, lead increases the risks for:"damage to the brain and nervous system, slowed growth and development, learning and behavior problems (e.g., reduced IQ, ADHD, juvenile delinquency, and criminal behavior), and hearing and speech problems."98z  

 

The American Academy of Pediatrics states, "low-level lead exposure, even at blood lead concentrations below 5 µg/dL (50 ppb), is a causal risk factor for diminished intellectual and academic abilities (and) higher rates of neurobehavioral disorders such as hyperactivity and attention deficits. No effective treatments ameliorate the permanent developmental effects of lead toxicity."

 

A 2015 study, summarizing results of earlier studies, states, "Even low-level exposure to lead that is prevalent in daily living has been associated with reduced intelligence, impaired attention, and behavioral problems."98z2  Experts have provided other authoritative evidence of adverse cognitive effects at very low levels of lead.98q14  In a 2006 study, major increases in ADHD were found even in children with blood levels below 2 µg/dL (2 mcg/dL, or 20 parts per billion). (see Figure 6.0c)  An earlier study showed no evidence of a harmless level of lead going down to 1 µg/dL98z3  According to Health Canada, "several studies have modelled a dose–response relationship that extends down to the lowest blood lead concentrations studied (1–2 μg/dL)."98z4  A study published in 2016 found that an average lead level of only 1.64 μg/dL was associated with more autistic behaviors.98q2  A 2009 study found elevated ADHD risk at lead levels in the 1-1.5 μg/dL range.98q20   Another 2016 study found lead levels as low as 1.2 μg/dL to be associated with increased ADHD.98q15

 

The above evidence indicating adverse effects of lead even at blood levels well below 2 µg/dL should be seen in light of CDC data indicating that 3% of U.S. children tested in 2015, even after decades of reductions in lead levels, had blood lead levels at or above 5 µg/dL98q4  The percentage of children with lead levels at or above the "below 2" μg/dL level is apparently not available, but it would clearly be far higher than 3%.  And it should be remembered that an American infant's lead levels during the 2000's would usually be determined mainly by breastfeeding (or not breastfeeding). (See Figure 6.0 above and accompanying text about how substantially transfers of lead via breastfeeding can contribute to an infant's lead levels.)

 

There is also considerable other evidence linking lead, in concentrations that are found in many infants in the contemporary U.S., with greater risk of autism (see Section 3.e.2.h) and ADHD (see Section 3.e.2.i).

 

 

Summary of a few points: 

-- Blood lead levels below 2 µg/dL have been associated in many studies with neurological impairments. (see above)

-- CDC data show that 3% of U.S. children in 2015 have blood lead levels at or above 5 mcg/dL,98q4 indicating that a very significant percentage would have lead levels in the range associated with neurological impairment.

-- Among infants breastfed for three months or more, which applies to most U.S. and European infants in the 2000's, the infants' blood lead levels will normally be mainly a result of breastfeeding. (see Figure 6.0 and following text)

--  It should be reasonable to assume that, largely as a result of breastfeeding, a significant percentage of  U.S. infants have lead concentrations in a known hazardous range.

 

 

3.e.2.d:  Lead accumulates in the body long-term98g and is mobilized during lactation:

 

A 2004 study cited four earlier studies as having "clearly shown that maternal bone stores of lead are mobilized to a marked degree during lactation."98d  Three other studies have also found postnatal increases in mothers' blood lead levels.98n, 99o 

 

 

3.e.2.e:  Major, rapid transfers from a grown person's accumulated lead to small infants: 

 

A 1994 study by a team of five researchers (Muldoon et al.), published in the American Journal of Epidemiology, found evidence of the large proportion of a woman's long-term lead burden that is transferred to her infant via breastfeeding:  In that study of 530 white women at ages 65 to 87 from Baltimore and rural Pennsylvania, carried out in 1990-1991, having breastfed was still associated with an average 11% reduction in women's lifetime accumulations of lead. 98s  Put another way, of the total stores of lead that a fully-grown body had accumulated over five to seven decades, loss of an average of 11% of that was associated with transfers to a woman's small, developing infants within a period of months.  Also, it should be noted that many or most of those women who breastfed would have been doing so during the decades when breastfeeding for six months was rare, a small fraction compared with the durations that have been typical in recent decades (see Figure 7 and the AAFP statement at 134); also, mothers were younger on average in those days, with fewer years for accumulating lead before transferring it to an infant.  The transfers of lead to infants by lactation these days would probably be significantly higher than the 11%-of-lifetime-accumulation figure above.

 

 Fig. 6.0a

leadInBM.gifLong-term blood lead levels in the elderly women in the study were also reduced merely in relation to having given birth, but they were reduced by only half as much as the levels in women who had breastfed; that was compatible with the prenatal-vs.-postnatal maternal blood lead levels shown in this chart (Fig. 6.0a) from another study.  Some maternal lead is transferred to the fetus, but far more is transferred to a breastfeeding infant.

 

Calcium is mobilized from the mother's bones to provide that nutrient to breast milk, but lead (being chemically similar to calcium) is mobilized from bone stores at the same time, and then deposited in breast milk.  In addition to the mothers whose data are shown here in this chart, all of the other mothers measured in this study (Manton et al.98m) also showed postnatal surges in their blood lead levels, surges that would be expected to show up in their breast milk; the increases continued for a longer period in women who breastfed for longer.  Two other studies showed similar results of major postnatal increases in maternal blood lead.98m1, 98m2

 

 

3.e.2.f:  Physical effects on the brain linked with childhood lead exposure:

 

Shown below are findings from a U.S. study98q by a team of 11 researchers who are authors or coauthors of a total of over 800 scientific articles.  They measured lead levels in young children (birth to 6.5 years) living in a poor area of a city "where there were many old, lead-contaminated houses." (Old houses are known to typically contain peeling, lead-containing paint.)  No mention was made of exposure to any other factors in this neighborhood that were likely to substantially increase lead exposure, such as industrial pollution.

          Fig. 6.0b

Male-female_leadEffec+.jpg 

 

 

The research group used magnetic resonance imaging to measure the brain volumes of the participants when they were 19-24 years old.  Brain loss associated with childhood lead exposure was very detectable, as shown in these brain images, and a dose-response effect was found; "the greatest brain volume loss was seen in participants with the greatest lead exposure in childhood." 

  

 

The blood lead levels that led to these effects on the brain were not extraordinarily high. Average blood lead levels of the children (13.3 μg/dl) were only one-third as high as the level at which signs of lead poisoning have normally been observed, 98q and also only one third as high as the maternal blood level that the CDC considers to be the maximum level at which the mother should breastfeed.98p2

 

 

As is obvious in the above chart, far greater effects were found in males than in females; this is significant in that disproportionately-high percentages of neurological disorders, as well as reduced academic performance, have been found in young males in recent decades.  For much more on this topic, including about male-adverse effects of the toxins discussed earlier in Section 3, see Section 7.

 

 

Average lead levels in the general population of children in the U.S. and other developed countries have declined greatly in recent decades as a result of public health measures, especially regarding leaded gasoline and paint.  However, summarizing from earlier in this section:  concentrated sources of lead in many mothers are continuing

-- a) in developed countries  in many occupations, hobbies and polluted areas;

-- b) in developing countries, where the lead-reducing public health measures are typically not yet in place; and

-- c) in most countries, lead is typically present in food, and women very often use cosmetics and/or ethnic remedies that are high in lead, and/or they often engage in pica-related ingestion of lead. 

 

Effects of all of the above would add up to hundreds of millions of mothers around the globe who are still heavily exposed to and accumulating lead.  The lead reduction that has taken place on average in children past infancy in developed countries in recent decades has been very significant, mainly reflecting reduced exposure to leaded fuel exhaust and peeling lead paint during childhood; but there appears to be no data about trends in lead levels of infants, whose lead levels would be largely determined by breastfeeding (see Figure 6.0 above and accompanying text), which has normally been increasing. (See Figures 7 and 8.aBear in mind that infancy is the period of greatest vulnerability to developmental toxins. (Section 2.d)

 

 

Section 3.e.2.g:  Effects of lead especially during the early postnatal period:

 

There appear to have been hardly any studies that tried to determine the period of maximum vulnerability to neurodevelopmental effects of lead during childhood.  But there are good reasons to suspect an especially early postnatal vulnerability, particularly compatible with sensitivity to lead transferred via breastfeeding, including

-- the statement by the neurology expert, D.C. Bellinger, that lead disrupts certain steps in formation of the brain, "affecting the processes by which neuronal circuitry is established;" included are "dose-dependent effects... on synapse (connection) formation," as well as many other adverse effects on the brain's developmental processes;93c notice in Figure 2 how much formation of the brain's critical circuitry, as well as development of the brain in general, takes place in the early months after birth;

--  the U.S. Public Health Service refers to the “early months after birth” as a “critical period” for development of the nervous system;93a

--  EPA researchers have stated that studies "have clearly demonstrated that when proliferation is actively occurring in a given region of the brain, it is vulnerable” to toxins.11  Remember again from Figure 2 the especially rapid proliferation that takes place in the brain during the year after birth.

-- A 1994 review article found that elevated blood lead at about age 2 had a significant adverse effect on IQ.  Only two other periods of vulnerability were considered in that study, as follows:  time-of-birth/prenatal lead had no observed effect, and preschool-years lead had less effect than lead levels measured at age 2. 98q7  So, considering that lead levels at age 2 are a result of accumulation up until that age, that study's finding of greatest sensitivity at age 2 (compared with 0 and 4) is fully compatible with adverse effects of lead ingested during the period of breastfeeding. 

-- Also see Sections 2.d and 9.b for considerable evidence of toxic effects of especially early postnatal exposures to toxins.

 

3.e.2.h:  Links between heavy metal (lead and mercury) exposure at levels often occurring in developed countries and autism:

 

 -- In a 2015 study in which 28 elements were measured in hair of 30 children aged 4-5 with ASD and 30 controls, lead was a standout in excess levels of contaminant elements, with excess concentrations of lead found in 78% of ASD cases and in only 16% of controls; mercury was in second place, with 43% of ASD cases having excesses versus 10% in controls.98p3

-- A 2013 study found significantly higher levels of all heavy metals (which include lead and mercury), ranging from 150% to 365%, in children with autism.98q8

--  In a 2009 study, body burdens of toxic metals were found to be significantly related to variations in the severity of autism, for each of four scales of autism severity.  The metal mentioned first among those having the greatest influence was lead.98q17

-- A 2011 study found highly significant (p=.001) elevations of lead and mercury in both hair and nail samples from children with autism.98q9 

-- As pointed out by the CDC, lead has been found to have adverse effects on children even at very low levels of exposure, and no threshold has been found below which exposure to lead appears to be safe.  In a South Korean study published in 2016, studying 2473 children, moderately elevated blood lead concentrations at 7–8 years of age were associated with more autistic behaviors at 11–12 years of age.  The blood lead concentrations of the group in which autistic behaviors were found in this study were at an average level of only 1.64 mcg/dL (micrograms per decileter). 98q2   This figure should be compared with CDC data indicating that over 3% of U.S. children in 2014 (over 100,000 children), even after decades of reductions in lead levels, had blood lead levels at or above 5 mcg/dL.98q4

-- Another 2011 study found significant elevations of lead in both hair and urine samples of children with autism, and significantly elevated mercury in urine samples.98q13

-- A 2005 study found significant elevations of lead and mercury in children with autism.98q11

-- A 2015 Egyptian study found that the mean levels of lead and mercury in hair of autistic patients were significantly higher than levels in controls.98q19

-- A 2012 study reported findings supporting "the historic evidence that heavy metals, especially lead play a role in the development of ASD," citing studies going back to 1976, and showing a mean value of mercury hair concentration seven times as high in children with autism as the reference range based on non-autistic children.98q12 

......................................

When reading about all of the associations of lead with autism (above) and with ADHD (below), bear in mind that an American infant's lead levels would usually be mainly determined by breastfeeding (or not breastfeeding) during the 2000's. (See Figure 6.0 above and accompanying text about how substantially transfers of lead via breastfeeding can contribute to an infant's lead levels.)

 

3.e.2.i:  Links between lead exposure and ADHD:

According to a study published in 2016,98q5 "most published studies with low lead exposure levels... in the past decade have shown that lead is associated with ADHD at levels between 2 to 4 μg/d" (citing 7 studies); the authors cited another 3 studies for associations of lead with ADHD at higher lead levels. Adding what was learned from their own study, the authors noted that "our study is consistent with most of the existing literature suggesting that the association between lead and ADHD-symptoms occurs at levels ≤ 5 μg/dL." (that is, at lead levels equal to or below 5 mcg/dL)   As noted above, CDC data indicates that over 3% of U.S. children in 2015 had blood lead levels at least as high as the levels that were associated with ADHD in many studies. 98q4 

 

A review article published in 2016, based on 18 studies, arrived at a conclusion similar to that of the above 2016 study and also included elevated lead levels as having been found to be autism risk factors.98q16

 

A study published in 2006, by a team of five researchers who are authors or coauthors of over 1100 published studies among them, drew on data from the U.S. National Health and Nutrition Examination Survey 1999–2002.  The authors concluded that "290,000 cases of ADHD among U.S. children 4–15 years of age are attributable to environmental lead exposure," if a causal relationship were to apply in this case, which they apparently considered to be likely.98q15

Figure 6.0.c

image040.gif

 

As seen in this chart from the above-described study, a significant dose-response relationship was found between childhood lead exposure and ADHD; a dose-response relationship is considered to be especially good evidence for causation.  Notice that the exposure categories in this chart indicate actual concentrations of lead within the U.S. child population as determined in the 1999-2002 NHANES survey; the exposures investigated here were not unrealistically high compared with what would be expected in a typical environment. 98q18  

 

In a 2010 U.S. study, "background-levels of lead exposure were associated with ADHD in a clinically characterized sample, at the lowest levels of blood lead ever studied in relation to ADHD, and in both parent and teacher reports....  Lead exposure is a plausible neurobiological candidate for involvement in ADHD."  The authors emphasized that the associations that ADHD was found to have with lead were "at population typical exposure levels." 98q18  A 2009 Korean study found 28% greater risk of ADHD among children with blood lead levels typical of common background exposures (1- 1.5 mcg/dl) compared with children with BLLs below that level.98q20

 

In addition to evidence from many human studies, a substantial number of animal experiments suggest that lead has causal ADHD-related effects on neurodevelopment.98q18

 

ButChildren's blood lead levels in the U.S. have been greatly declining while ADHD has been increasing.  That conflicts with lead's being a cause of ADHD.

 

True, at least for the first sentence in bold.  On the other hand,

  a) Nobody says that lead is the only cause of ADHD.  There have also been substantial findings of associations between ADHD-related traits and exposures to the three organohalogen compounds discussed earlier; the specific implicated chemicals have been PCBs (see above Figure 4), dioxins (see Section 3.c), and brominated flame retardants (see this part of Section 3.b).

  b) Remember that all three of the ADHD-implicated toxins mentioned just above have been authoritatively found to be present in typical human milk in concentrations greatly exceeding established safe levels, while being at very low levels or absent in infant formula. (see early parts of Sections 3.a, 3.b and 3.cThen note that breastfeeding, especially for longer periods, has increased dramatically in recent decades (See Figure 7), greatly increasing transfers of those three toxins to infants. 

  c) The child blood lead levels for which there is evidence of a declining trend (using data from the U.S. CDC) are all measured in children one year old and older.  The previously-high levels in the over-1-year-old children were found to have been largely results of ingesting particles of lead-containing paint and long-term exposure to leaded gasoline emissions, both of which have declined greatly following public health measures of recent decades; we know that blood levels of children over age 1 have declined, as should have been expected.  But there appears to be no data for trends in lead levels of infants.  Those levels have resulted mainly from transplacental transfer and lactational transfer, and there can be no doubt that transfers via lactation in general have increased dramatically in recent decades. (see Figure 7, especially the line for breastfeeding at six months)  It is entirely possible that lead levels in infants, especially during the highly developmentally sensitive early months after birth (see Section 2.d) have increased greatly in recent decades.

 

 

 

Section 4:  Studies that have found prevalence of autism to correlate with breastfeeding:

 

In addition to the associations between the toxins discussed above and specific symptoms, several studies have found links between the main pathway for ingestion of those toxins by infants (breastfeeding) and autism.

 

 

Section 4.a:  Studies finding positive correlations between autism prevalence and breastfeeding duration:

 

Section 4.a.1:  Direct Links:

A 2011 study that investigated data from all 50 U.S. states and 51 U.S. counties found 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." 116

 

 

Note that, according to the EPA, Epidemiologic studies of exposed human populations provide the most convincing evidence of human health effects.”145a  Also, a dose-response relationship between an exposure and a health outcome is considered to be especially significant evidence to support a finding of cause and effect.  One example of a dose-response relationship, as found in a study by a well-published scientist (R.J. Shamberger), was quoted in the previous paragraph.  This finding was even more significant in that it was based on investigation of a very large, diversely-populated geographic area (all 50 U.S. states), and it also applied in relation to numerous smaller-scale units (51 counties). 

 

Additional support for a causal connection between breastfeeding and autism was provided by three additional, relatively recent studies, with a dose-response relationship being apparent in the different degrees of correlation with autism according to the different durations of breastfeeding, when these three studies are seen together.

-- In a 2011 Canadian study of a population of over 125,000, using discharge from the hospital as the dividing line for breastfeeding exposure, there was a 25% higher autism rate among the breastfed children than among non-breastfed children.117

-- In a 2009 U.K. study, the duration of breastfeeding that was assessed was four weeks versus less than that, with 65% of the autism cases having received breastfeeding for at least four weeks; that should be compared with only about 28% of the general U.K. infant population (where breastfeeding rates are relatively low) receiving that much breastfeeding; that meant a 130% higher-than-average likelihood of that much breastfeeding history among those with autism. 118

-- In a 2010 American study in Kentucky by two MD’s, the duration of breastfeeding used for comparison was six months, and 37% of autism cases had received that much breastfeeding, compared with 13% of the controls, indicating an approximately 185% (37%/13%) greater likelihood that the autism cases would have had more breastfeeding; the p-value was .003, meaning three chances out of a thousand that the finding was a result of chance occurrence. 119

.................................................

 

Section 4.a.2:  Studies that indirectly link breastfeeding with risk of autism:

In this subsection, studies will be presented that did not directly investigate breastfeeding as the exposure in relation to autism as the associated outcome, but what is examined is just a close step or two away from that; it requires little mental effort to see valid connections between the breastfeeding-related exposures and autism-related outcomes.

 

Section 4.a.2.1:   Breastfeeding associated with autism-related traits:

 

A 2013 study in Taiwan (Lung et al.119g) worked with data from over 21,000 children, 953 of whom lived within three kilometers of a municipal incinerator.  The authors reported about effects of local incinerators on children in the general population, as indicated by parental concerns in specific developmental areas and at certain ages.  The study's general results showed that, out of twelve questions regarding parental concerns about neurological development, responses to only one question showed significantly greater concern among parents of children who lived closer to incinerators than among parents of children who lived farther away. 

 

However, by going well past the end of the study's text and looking carefully in the supplementary material, one can read about greater adverse effects on breastfed than on non-breastfed children, as follows:  "Through the mediating factor of breastfeeding, the presence of an incinerator was indirectly associated with six-month gross motor (β = 0.02, p = 0.003) and fine motor (β = 0.02, p < 0.001) development and 18-month gross motor (β = 0.02, p = 0.011), fine motor (β = 0.04, p < 0.001), language (β = 0.03, p < 0.001) and social (β = 0.05, p < 0.001) development."

 

To state the gist of the above two paragraphs in simpler terms:   According to parental reports, the following comparisons were apparent:

   a) adverse effects from the local incinerator on measured outcomes in four times as many developmental areas and six times as many separate questions, in breastfed children compared with children in the general population; and

   b) much more pronounced effects (many times greater statistical significance), in breastfed children compared with the effect seen in children in the general population, in five of those six areas.  See how low those p values are in the figures quoted above (lower = less likely to be a result of chance variation), and compare them with the p value of .008 for the one area in which there was significant effect of local incineration on children in the general population.

 

The following points are especially noteworthy in this study:

   a) All of the areas in which breastfed children were seen to have worse development were areas that are traits of autism:  deficits in social development are a core characteristic of ASD, and language impairment and clumsiness are common traits of those with ASD.119h

 

   b) Breastfed children were considered to have worse development in all areas that the study looked into, at the latest age for which results for breastfed children were reported.

 

   c) Breastfed children were considered to have only half as many developmental problems at the earlier (six-month) age as they had at 18 months; this parallels the typical emergence of traits of autism during the early years after birth, with symptoms normally being unobservable in the earliest months and becoming detectable later.

 

   d) The authors, very possibly responding to pressure from peer reviewers and publishers, appear to have gone to great lengths to minimize noticeability of their data showing the adverse effects of breastfeeding that were found in their study; that information was placed well past the normal reading area of the study, after the extended listing of footnotes, with no clues in the main text about other significant data being available to be found somewhere else; when the data can finally be seen following an unusually resolute search, it is inconspicuously located in the middle of a paragraph about "residual effect of development at six months."  There is no heading and not even a topic sentence indicating that a noteworthy finding was within that paragraph.

 

It is safe to say that, if an exposure being studied is found to have many times greater effects on one subgroup than on the general population being discussed, that finding would normally receive prominent attention in the body of a study.  But the very opposite occurred in this case.  The near-concealment of the outstandingly adverse effects on breastfed children, specifically, could be an indication of biases among researchers, among people in the publishing field, and/or in research funding agencies.  Publication bias is well accepted as being a serious concern in scientific research.  The U.S. government's strongly-held, one-sided pro-breastfeeding position (such as can be seen  at www.womenshealth.gov/breastfeeding) makes it apparent why researchers who want to please this dominant source of research funding (the U.S. government) would typically be very reluctant to publish findings that indicate adverse effects of breastfeeding.

 

One can only wonder how many other findings about adverse effects of breastfeeding have gone unreported or have been essentially hidden from normal view, given the intense competition for research grants and the challenges of getting research published.

 

........................................

 

It may be reasonable to question the validity of the parental concerns that were the basis for data about apparent adverse effects on breastfed children, in the above study.  But this was far from the only study that has found autism-related effects of breastfeeding:  Remember the four studies that have found links between breastfeeding and diagnosed autism, in dose-response relationships (above in Section 4.a.1);

 

PCBs, PBDEs, mercury, and lead are included among chemicals that are part of normal municipal waste matter that would go into an incinerator, especially in discarded electrical fixtures and electronics (PCBs, PBDEs and lead), old painted products (lead), discarded medical items, appliances and light bulbs (mercury), etc.  All four of those chemicals have been found in potentially hazardous concentrations in average human milk (see Section 3); it would be reasonable to assume that those chemicals would be present in higher concentrations in milk of mothers living closer to airborne sources of those chemicals, such as incinerators.

 

Also bear in mind that many chemicals from the environment are known to become concentrated by the lactation process before being ingested by infants at a time of high developmental vulnerability.  Studies respectfully summarized in a publication of the U.S. National Academies Press indicate that infant exposures to PCBs via breastfeeding have been found to be hundreds of times greater than prenatal exposures.18  A commission of the German Federal Environmental Office reported that the average daily PCB intake of an adult is 0.02 micrograms per kg of body weight, as compared with the intake of a breastfed infant (3 micrograms per kg of body weight), which is 150 times higher.18a  Other studies have observed that nursing infants consume a daily TEQ (toxic equivalency -- normally used in reference to dioxins) intake that is 50 times higher than that of adults.18b   A 1998 study of 330 mother-infant pairs found that "breast-fed infants of smoking mothers have urine cotinine levels 10-fold higher than bottle-fed infants whose mothers smoke."18c (Cotinine is a marker for smoke exposure)  Remember from earlier that, even at 11 months of age, dioxin toxicity-equivalent concentrations in breastfed infants were found to be about 10 times higher than in formula-fed infants.79  Considerable other evidence can be found in Section 2.b and in Appendix G concerning lactation's property of concentrating toxins in the process of transferring them to infants.

 

Developmental exposures to the chemicals that would be emitted from incinerators (discussed above), which would then become concentrated by lactation, have been linked in many studies with neurological deficits, including ones that are related to autism.  (see Section 3)

 

....................................................

 

Section 4.a.2.2:

 

(a) Breast milk is the predominant pathway for pesticides to most infants, at a stage of high developmental vulnerability;  

 

 

(b) fairly common pesticide exposures are closely linked with autism risk, in many studies.

 

 

 -- Should we think about (a) and (b) at the same time?

 

 

There have apparently been no studies that have investigated associations directly between autism and ingestions of pesticides via breast milk; but logical combinations of studies enable us to see a real link between that exposure and that endpoint.  Below it will be pointed out, based on authoritative sources that are cited, that human milk is the predominant pathway for pesticides to most infants, and in very significant doses; but first the following:

 

Substantial evidence linking common pesticide exposures with origins of autism:

  a)  When summarizing data from 37 unique studies, the authors of a 2014 review article (Rossignol et al.) found that 34 studies (92%) reported an association between estimated exposures to environmental toxicants and ASD.  Most of the reviewed studies were said to have had good study designs, and the toxicants that appeared to have the strongest association with ASD were pesticides and air pollutants.139 (emphasis added)  

 

  b) Another  2014 review article generalized concerning effects of pesticides that "most give rise to neurotoxicity."137d Based on seven epidemiological studies determined to be of high quality, elevated risk of autism associated with pesticide exposure was found "with large enough impact and statistical precision to rule out sampling error."

 

  c) Since there have been so many different studies of human populations that have found associations between pesticide exposures and autism prevalence, that strongly implies that the autism-linked pesticide exposures are widespread, not isolated poisonings; bear in mind that pesticide levels in the breast milk of urban mothers have been found to be similar to levels in milk from mothers in agricultural areas.141

 

  d) In a 2007 study, autism prevalence was found to be six times as high as normal near California agricultural fields where organochlorine pesticides were applied; autism prevalence varied in correlation with distance from the fields and with poundage of pesticides applied.136 

 

  f) A 2012 study found that the time of peak correlation of pesticide exposure with autism incidence (in the study described just above) was in the year after birth;137  a correlation with the year after birth directly implicates exposure via breastfeeding, especially in communities with high breastfeeding rates such as in the above study, for reasons that will be presented below the next bold heading.

 

For additional evidence on this topic, see Appendix F.

 

Evidence indicating that infant exposures to pesticides are normally significant and are predominantly received via breastfeeding:

 

1) Experts stated in 2006 that specific pesticides ... 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. 139e (Many or most pesticides, including the major organochlorine and organophosphate types, are lipophilic139g (attracted to fat) and therefore become concentrated in breast milk.139f)  

 

2) In what have apparently been the major published studies about pesticides contained in human milk (in Denmark, Finland and the U.S.), many different pesticides were found in the milk of over 90% of all women, in urban as well as agricultural areas; the average pesticide concentrations were over 10 times the lowest concentrations measured.  This compares with no pesticides found in over 99% of all samples of infant formula. (See Section 8.a for much more on this topic, including citations of sources.)

 

3) According to the U.S. National Research Council, "The gastrointestinal tract is the major portal of entry of pesticides into the body."139h

 

4) A 2011 study examined many different “exposure prediction factors” that could contribute to children’s levels of metabolites of organophosphorous pesticides; the authors found that, at six months of age, current breastfeeding was a stronger predictor of exposures to this major group of pesticide types than eleven other factors considered.139a  The only factors that were stronger predictors (child care less than 60 meters from an agricultural field and home use of pesticides during the previous six months) applied to only small minorities of the children studied (6% and 2%).  Therefore, for the vast majority of young infants, current breastfeeding was found to be the strongest predictor of their levels of exposure to a major group of pesticides, among the many possibilities that were considered. 

 

  

To summarize briefly:

(a) Breastfeeding is very probably the predominant pathway for transfers of pesticides to infants;

  

(b) those exposures to pesticides are significant and come during infants' vulnerable developmental periods;

 

(c) pesticides in infants are important risk factors for autism, by substantial evidence.

 

Progression from (a) to (c) above, from breastfeeding through to increased autism risk, appears to be very well supported by evidence, as indicated earlier.

 

There has apparently been no study published that has directly measured the correlation between pesticides transmitted via breastfeeding and risk of autism; but connecting a few dots should enable one to see a strong connection there.  That is especially true given the strong associations between breastfeeding and autism as indicated in the studies in Section 4.a.1.

    

 

For information about effects of pesticides in increasing risk of ADHD, see Section 8.b.2.

 

 

Section 4.b:  Autism and toxins in breast milk both decline greatly in relation to birth order. Those two declines’ taking place in parallel might not be a coincidence.

 

In a 2008 American study by eleven scientists, studying a birth cohort of over 250,000, a typical fourth child’s risk of autism was found to be half as high as that of a firstborn, and the odds of being diagnosed with autism decreased from first to later children.120  A California study121 and a major study in Australia122 provided general confirmation of the above relationship.

 

Probably related to the above:  The average duration of breastfeeding is greater for earlier-born children than for later-born,123 and milk received by later-born infants has toxin levels that have been found to be half as high as milk received by first-borns, as a result of excretion of long-term accumulations to earlier-born infants during previous nursing.124

 

Other studies provide additional confirmation of the above. Data from the U.K. Department of Health for 1995 shows a 17% decline in breastfeeding rate between the first and later births,125 and a Canadian study had compatible findings.126  Similar results regarding decline of toxins in breast milk with birth order have been found in other studies, especially regarding dioxins and PCBs, in the U.S.,127 U.K.,127a Germany,128 and Norway,129 and regarding mercury in Saudi Arabia. 85c   Also see the Ennaceur et al. study, the source of the chart below, as well as the 2002 study described below that chart.

 

At a quick first glance, the chart below could be a graphical representation of the decline that has been found in autism rates according to birth order.120

 

Fig. 6.a

http://www.pollution-effects.info/index_files/image014.gif

 
 N

Neurological toxins typically ingested in infancy decline with birth order, as indicated above and in the text above this chart.  The close resemblance of this decline to the decline in autism by birth order120, 121,122 might not be coincidental.

 

 

………………….

 

 

A study published in 2002 looked into concentrations of dioxins that were measured in various tissues of 27 infants that had died unexpectedly; it was found that the closer the infant had been to first in birth order, the higher the dioxin concentrations in the deceased infants’ tissues, “thus showing” (as stated by the study’s authors) “that the mothers can decontaminate themselves by breast feeding.”130  (See in the chart above additional evidence of reduction of a mother's accumulations of toxins with each additional course of breastfeeding.)  Considering the obvious benefits of the mother’s clearing out much of her lifetime accumulations of dioxins by transferring them to her infant, the reader should remember that, when referring to the “particularly devastating” effects of dioxins and PCBs, a major toxicology textbook also points out that “the most susceptible period of exposure is during development and nursing.”131  Clearly, feeding a grown person’s long-term accumulations of dioxins to a vulnerable, developing infant is to be recommended since, as stated by the authors of the study, various physicians’ associations recommend breastfeeding.  No mention is made of the fact that, when repeatedly asked how they have determined that the toxins in human milk are not causing harm that outweighs the benefits of breastfeeding, those associations never respond. 

 

....................................

 

Section 4.c:  Studies that have associated autism risk with less breastfeeding:

Promoters of breastfeeding typically point to a study carried out in the Sultanate of Oman (Al-Farsi et al.), another in which the participants in a parent-created survey responded to Google ads (Schulz et al.), and a 1989 study in Japan that found earlier weaning among infants who would later be diagnosed with autism (Tanoue et al.). This is not exactly an impressive array of contemporary, professionally-conducted studies that could be generalized to conditions in most countries; but a closer look shows it to be even worse. The Tanoue study is an excellent example of likely reverse causation; there is ample evidence indicating a strong likelihood that emerging autism would cause early weaning, rather than causation being in the opposite direction as some people surmise based on that study:

--  Of only 16 mothers in a U.S. study who breastfed infants who were later diagnosed with ASD, "several" reported physical trauma as a result of their infants' overly-persistent sucking, which the authors related to the persistent, repetitive behavior that is a diagnostic of ASD.119d

--  Women often give "sore, cracked or bleeding nipples" and "breastfeeding too painful" as reasons for discontinuing breastfeeding; 119b that could well result from the activity described just above, on the part of babies who will later be diagnosed with autism. 

--  One study carried out a systematic review of other studies that investigated "severe irritability" and problem behaviors among those with autism;119e the publication of so many studies on that topic implies that behavior that would conflict with agreeable breastfeeding could be a common characteristic of babies who are developing traits of autism.   

--  A 2013 study found that children with ASD were "five times more likely to have a feeding problem, including extreme tantrums during meals, (and) severe food selectivity." 119c

--  Note that infants who were later to be diagnosed with autism were found to have sucking behaviors that created problems for the mothers within two weeks after discharge,119d and early changes specifically linked with autism have been observed (by advanced technology) to begin within two months after birth;119f unpleasant traits of autism could well be emerging soon enough after birth to cause early weaning.

 

Another study (Burd et al., 1988) is sometimes provided as evidence to indicate benefits of breastfeeding in relation to autism; a proper response to that is somewhat lengthy, so our response to that study can be found at the end of www.pollutionaction.org/comments.htm

 

If anyone can provide any other studies that imply benefits of breastfeeding with regard to autism risk, please send them to dm@pollutionaction.org and they will be posted here, along with our response.

 

.....................................

 

Although the focus of this article is on neurological disorders, the following should be mentioned regarding general developmental problems:

   a) essentially all of the studies finding benefits of breastfeeding have been of a type that leading authorities on medical evidence consider to be of low quality (see observational late in Section 10); and

   b) over 50 studies (in addition to those cited above) have found adverse health effects of breastfeeding, often including dose-response effects. (see www.breastfeeding-studies.info)

 

 

 

Section 5:  There have been major increases in breastfeeding in parallel with major increases in child disorders; the increases were very rapid for a decade or so and slower later, in the cases of both breastfeeding and the child disorders.

 

 

Fig. 7

 

 

http://www.pollution-effects.info/index_files/image011.gif

 

 

Following a moderate increase beginning in 1965, and a rapid increase after the early 1970's, overall growth of breastfeeding in the U.S. has been very large, especially in extended and exclusive breastfeeding. Breastfeeding for at least six months increased ten-fold from 1971 to 2007.

 

Bear in mind that this greatly increased feeding type is apparently the predominant pathway of infant exposure to each of several developmental toxins, in high concentrations (see Section 6 below).

 

As can be seen in the above chart, increases in breastfeeding rates were especially rapid from 1972 to 1983, followed by much slower growth after that.  Disabilities in American children followed that same pattern, with especially rapid increases in disabilities among children born between the early 1970’s and the mid-80’s (see Figure 11 and accompanying text) and much slower increases in later years;113a a CDC statement of 2008 reported that the more recent rate of increase in enrollments in special education for specific learning disabilities was less rapid than it had been earlier, following the “marked” increases of the 1970’s and 1980’s.108a

 

Note that the increases in relation to the 1970 breastfeeding rate were especially dramatic in the case of longer-term breastfeeding

 

Remember that

  (a) the above-discussed transfers to infants take place at a time of the developing brain’s known vulnerability to such toxins (see Section 2);

  (b) typical breast milk contains four different developmental toxins in concentrations that far exceed established safe levels, plus lead and numerous pesticides, while the principal alternative feeding contains little or none of those toxins (see Sections 3 and 8); and

  (c) most of those types of toxins have been found to either reduce scholastic achievement specifically of males or to reduce hormones that are important to neurological development and motivation specifically of males; (see Section 7.a.2)  males are the sex that is much more affected by ADHD, autism, and some other increasingly-diagnosed disorders. (see Section 7)  

 

There is much more indicating that the parallel increases of breastfeeding and child disorders might not have been merely coincidental; see Section 9.

 

……………………………

 

 

In addition to major increases in what is probably the predominant pathway of developmental toxins to infants (breastfeeding -- see above and Section 6 just below), concentrations of some major toxins were also rapidly increasing in the environment and in human milk during those years:  PBDE levels were doubling in humans approximately every three to five years during most of the period discussed here,114d  and HBCD levels have been rapidly increasing well into the 2000’s. (see Figures 5.1 and  5a and accompanying text)

 

 

 

Section ­6:  A possibly unique pathway of widespread infant exposure to developmental toxins in doses exceeding established safe levels:

 

As described in Sections 3, with considerable authoritative supporting evidence, breastfeeding is a pathway for ingestion of multiple developmental toxins by infants, four of them at especially high levels.  But it is more than just a pathway; it may be the only pathway by which infants are widely exposed to any developmental toxins in doses exceeding established safe levels. The author of this article has written relevant letters of inquiry to

a) the American Academy of Pediatrics,

b) the American Academy of Family Physicians,

c) the entire science team at the major autism-advocacy organization, Autism Speaks;

 

those letters asked about awareness of any toxins that are believed to widely reach infants in doses well in excess of a recognized safe level (e.g., EPA’s RfD), aside from the four such toxins that are ingested by means of breast milk.  As of three or more months later, none of the four replies that were received suggested any other such toxins.

 

Related to this are the very large differences between concentrations of toxins in breast milk and those in the main alternative infant feeding.  The toxins being discussed here are present in infant formula in concentrations less than 7% as high, and usually less than 1% as high, as their concentrations in human milk. (See near the beginnings of Section 8 and each of the subsections of Section 3 above; a summary in one place is Section 2, cont. of www.disability-origins.info.)

 

 

 

 

Section 7:  Effects of all of the above developmental toxins specifically on male children, who are very disproportionately diagnosed with neurological disorders as well as falling behind in education:

The very high ratios of males to females among children affected by the increasing neurological disorders99a, 112a (especially ASD and ADHD) have been basically unexplained.  Disproportionate problems among boys have also reached well into the general population, far beyond those with diagnosed disorders, again with nothing but speculation as to the cause of this disparity.

 

Section 7.a:  Problems of boys and young men in education and life; most of the toxins discussed here have been scientifically observed to have sex-specific effects on male learning ability, male capacity for higher cognitive processes, and development of the male brain:

 

Section 7.a.1: Problems of boys and young men in education and life:

As indications of the high percentages of mental problems in males in the general population in recent decades, the following are quotations excerpted from titles of books in recent years:

 -- The Trouble with Boys, a Surprising Report Card on our Sons, their Problems in School… (2009) (a New York Times best seller) by Peg Tyre;

 -- The Minds of Boys: Saving Our Sons From Falling Behind in School and Life, by Michael Gurian (2007);

 -- Why Boys Fail…, by Richard Whitmire (2010); (Chosen by The American School Board magazine as one of 2010's Top Education Reads). From a description of the book, “Boys are falling behind in school… Even in their traditionally strong subjects of science and math…. The gap between male and female achievement has reached the college level, where only 40 per cent of graduates next year will be male.”

 -- Boys Adrift: The Five Factors Driving the Growing Epidemic of Unmotivated Boys and Underachieving Young Men (2009) by Leonard Sax, MD, Ph.D.;99d favorably reviewed by the Journal of the American Medical Association. (Note that the central word in the title is not “trend” or “increase,” but something much more serious:  epidemic.)

 

A 2006 article in the New York Times, headlined “At Colleges, Women Are Leaving Men in the Dust,” refers to a “new emphasis on young men's problems” as indicated in magazine covers and talk shows at that time, and quotes the director of the Centers for Men and Young Men at McLean Hospital/Harvard Medical School as saying "They have a sense of lassitude, a lack of focus."99h

 

Quoting from a 2013 article in The Atlantic, “…boys are languishing while girls are succeeding,” and College admissions officers were at first baffled, then concerned, and finally panicked over the dearth of male applicants....”99e  Such problems are also widespread among the 34 countries of the Organization for Economic Co-operation and Development.99k  An official of that organization referred in 2016 to “low achievement among boys, often combined with a lack of motivation….”99g

 

There is considerable speculation as to why all of this has been occurring, but nothing has gotten past the level of conjecture.99f

 

When seeking an underlying cause, it would be helpful to look for the approximate time when the adverse mental trend for boys and men may have originated, which is likely to have been during the boys’ early developmental periods; there is substantial evidence about vulnerability of early-postnatal mental development to toxins, as indicated in Figure 2 and accompanying text.  One author stated in a 2000 Simon & Schuster publication, “In the late 1990s… articles about boys' educational deficits began to appear in American newspapers with headlines (such as) ‘U.S. Colleges Begin to Ask, Where Have the Men Gone?’"99m Since a typical college student would be approximately 18 to 23 years old, it would therefore be logical to look back from the late 1990's to the mid-to-late 1970’s for the birth years of the boys who would later have been at typical college age when those articles about boys' educational deficits began to appear. There is also other evidence, based on college completion data from the U.S. National Longitudinal Survey of Youth, which is compatible with this period as constituting the birth years of the males whose percentages were declining in the college scene in the late 1990’s. (see chart in reference 99n)

 

So the mid-to-late 1970’s would be especially worth looking at for any toxic exposures that might have been appearing in the environment during the years when the brains of those boys would have been at a vulnerable stage of development.  See Figure 7 about rapid growth of breastfeeding rates during that period; human milk is clearly a major source of infant exposure to pollutants from the environment (see Section 3).  Although promoters of breastfeeding usually do not acknowledge the seriousness of the effects of the contaminants in breast milk, apparently nobody knows about existence of any other major pathway for developmental toxins to infants in doses exceeding established safe levels. (see Section 6).

 

 

Section 7.a.2:  Toxins discussed here have been scientifically observed to have sex-specific effects on male learning ability, male capacity for higher cognitive processes, and development of the male brain: 

 

 

It is of interest to see what was observed in a 2009 study by seven Italian researchers (Colciago et al.99o) about effects of developmental exposure of rats to PCBs, one of the toxins that are typically in high concentrations in human milk in developed countries, as discussed in Section 3.  

Fig. 7.a

http://www.pollution-effects.info/index_files/image016.gifThe PCB exposures of the rats were in doses that did not cause general toxicity in the animals.  After the rats reached adult age, a test of learning ability was conducted with four groups:  males and females that had been developmentally exposed to PCBs, and males and females that had not been exposed (control groups).  In the first step of that test, the rats stepped into a dark compartment and received a mild shock.

 

A day later, when again near the entrance to a dark compartment, those rats’ learning from the previous experience was indicated by how long they hesitated before entering such a compartment again. In the chart on the left, the results from the four groups are shown in four pairs of bars. There had been only brief delays before first entering, as shown in the left-hand bars in each pair.  The lengths of hesitations before entering a dark room on the next day are shown in the right-hand bars; those next-day delays clearly varied considerably according to sex and exposure.  As can be seen here, both of the unexposed groups had learned from the previous day’s experience to be very cautious; and the exposed females also remembered well enough to be very cautious; but only the males that had been developmentally exposed to PCBs essentially forgot their experiences of the day before. 

 

A 2016 experiment with rats indicated effects of low-dose developmental exposure to methylmercury, as follows:  The exposed rats displayed normal locomotion and motor coordination, but male rats had “learning disturbances” and “a predisposition to depressive-like behavior.”  The female rats showed no such changes.99s 

 

A 2015 study with mice illustrated the neurological harm that may be caused by a widely and increasingly-used residential pesticide (of the pyrethroid type), with far greater effects on males than on females.  (see chart below)

Figure 7.a1

image041.gif

 

The P values shown are a statistical indication that there is one chance out of 1000 that the adverse outcomes following developmental exposure to the pesticide, regarding male impulsiveness, memory, and attention, were results of chance.

 

....................................

 

The question obviously comes up as to whether these toxins have the same effects on humans that they had in the animal experiments.  With regard to pyrethroid pesticides, a 2015 study using human data (from the NHANES survey) found that boys with detectable levels of this pesticide were almost three times as likely to have ADHD as boys who had non-detectable levels of pyrethroids, while in girls the increase was less than one-fifth as high.99w

 

There is also ample evidence indicating that the other toxins discussed here have the same effects on humans as they have in animal experiments -- see Section 3.a concerning effects of PCBs and Section 3.d concerning effects of mercury. When the study results are broken down by sex, they seem to show the same kinds of sex-specific effects as were shown in the animal studies See the review charts just below, and/or go to the original charts and accompanying text for more information.  Also,  see "Additional studies" farther down for more studies showing specifically male-adverse effects of these toxins in both human studies and animal experiments.

 

Abbreviated review of Figures 6 and 6.0b

review2pixj.jpg

 

 

Regarding the PCBs, mercury and pesticides discussed above, it is relevant that typical exposures of human infants via breastfeeding have been in doses far exceeding the relatively safe doses established by U.S. government agencies (in the cases of PCBs and mercury),23, 82 or typical exposures of breastfed infants have at least been substantial (in the case of many pesticides) 140, 141. The principal alternative infant feeding, which apparently worked well for the U.S. generation born in the mid-20th century (see alternative in Section 10), has been found to contain either none or extremely little of those toxins.30, 75, 83 (also see Section 8.a)

.........................................

 

Remember that the process that results in high infant exposures to these toxins was rapidly increasing in popularity in the U.S. during the 1970’s (see Figure 7), at the very time when boys were being born and developing who would later be at the beginning of the greatly increasing problems of males in education.

 

Also remember that the physicians’ associations that promote breastfeeding, when asked how they have determined that the benefits of breastfeeding outweigh the risks, never respond.

 

 

Additional studies finding male-adverse neurological effects of toxins that are high in human milk:

 

In a 2016 Chinese study of postnatal exposures of human children to typical contemporary (organophosphorous) pesticides, strong adverse neurological effects were found in males, compared with little or no effects in females.  The male-to-female ratios for developmental delay in the motor area of children with higher concentrations of  two of the pesticide metabolites were about 150 to 1 and 50 to 1.  The adverse effects of postnatal concentrations of one pesticide on the social area of males was over five times greater than the similar adverse effect on females.99t  

 

Effect of mercury on signal transmission within brains of males only:   A 2007 animal experiment (Coccini et al.99p) tested the effects of two common developmental toxins on certain receptors (MRs) that are present in the brains of both humans and rats, which enable transmission of signals between neurons. According to the authors, “these receptors are known to play a major role in many central functions including higher cognitive processes….”  Methylmercury had an effect of causing long-term decrease of MRs in one major part of the brain in male rats only; and PCBs led to a (delayed) decrease of MRs in another important part of the brain, again in males only.

 

Effects of PCBs, at background-exposure levels, in distorting the structure of the male brain, with less or no effects in females:  A 2005 animal experiment (Nguon et al.99r) exposed developing rats to PCBs in doses that the authors considered to be “likely to result in PCB levels comparable to PCB levels found in the blood of Belgian children” as well as similar to levels in the blood of children in a study carried out in the U.S. Great Lakes region.  Measurements were taken of the rats’ cerebella, which were of special interest because problems in the cerebella in human brains have been extensively associated with autism (see Section 4.a of www.disability-origins.info); in the exposed rats on postnatal day 6, the sizes of the females’ cerebella were not affected by the toxins, compared with controls, but the cerebella of exposed males were reduced by 14.3%, compared with control males.  Another change in the brains that was measured in connection with the PCB exposure, alteration of “L1” proteins (which are present in both human and rat brains) was four times as great in male brains as in female brains. Remember that these distortions in the brain, affecting males very disproportionately, followed developmental exposures to PCBs that were comparable to exposures found among substantial numbers of contemporary human children. And bear in mind the extreme differences between exposures to PCBs of breastfed versus non-breastfed infants while the brain is developing (see Section 3.a).

 

 

See Section 7.b.3 and 7.b.4 later about effects of PBDEs in reducing hormones that are important for human male mental development and function.

 

………………………

 

Aside from gender-specific direct effects of these toxins in leading to learning disability and other abnormalities in males as indicated above, there is also considerable evidence about indirect effects of environmental toxins in human milk on motivation and attention of males; these are the other major deficits observed in boys and young men in recent decades.  Much of Section 7.b, just below, deals with this topic.

 

 

 

Section 7.b:  Effects of these toxins on male motivation and attention via reduction of certain hormones:

 

 

As will be explained shortly, most of the toxins discussed here reduce levels of testosterone, which would clearly have effects mainly on males.  Importance of testosterone to male motivation and mental functions will therefore be explained here.  According to Dr. Edmund Sabanegh, chair of the urology department at the Cleveland Clinic in Ohio, testosterone “…keeps men running. Diminished mental clarity, motivation, drive -- all of these things can be related to low testosterone."103a A publication of the Endocrine Society, the largest organization representing professionals from the field of endocrinology, says essentially the same thing.103b  As will be explained a little later, testosterone supply in youth and in adulthood, and its mental effects, are greatly influenced by effects of the toxins that are being discussed here.

 

A 1991 study arrived at findings indicating importance of testosterone to attention, another trait that is obviously also important to progress in education.  Quoting from that study, “Considerable evidence suggests that testosterone (has)… effects on attention in mammals.” And also, “reduction by testosterone of distractibility by irrelevant stimuli has been demonstrated in tests” in three different types of animals.103c

 

Aside from their importance to motivation and attention, sex steroid hormones are also important to neurological development and male mental functioning in general:   According to one expert, "Sex steroid hormones play a role early in brain development…  A wide variety of neural processes are influenced by sex steroid hormones, including neurogenesis, …growth of the neuronal cell body… synapse formation….and neuronal excitability."99b  (italics added)   According to another expert, ”Gonadal, adrenal, and thyroid hormones affect the brain directly, ….any agent that disrupts normal hormone secretion can upset normal brain development."99c  Other experts on neurological development point to testosterone, specifically, for the way it "clearly affects brain development;" they refer to the "critical period for the testosterone organizational effect" that takes place when the brain is developing.102

 

Since testosterone is

1) important to male neurological development as well as to later motivation and attention (see just above),

2) a predominantly-male hormone, and

3) vulnerable to reduction by developmental toxins to which infants have been very increasingly exposed in recent decades (see Sections 4.b.1- 4.b.3 earlier and also Figures 8.a and 7),

 

we should consider the possibility that reduced testosterone levels may underlie the recent problems of young males in education, as well as the increases in (the mostly-male) ADHD.  

 

Declines in testosterone and testicular function in recent decades:

 

A web page of the American Physiological Society refers to a study being published in 2016 (Skakkabaek and 13 others), by “a team of experts in reproductive medicine from Denmark, Finland and the U.S.” in which the authors observed lower levels of testosterone in men.”  The first author of the study was quoted as saying (in reference to recent signs of subnormal function of male sex glands), “I was surprised that we found such poor semen quality among young men ages 20 to 25.” 103f  A 2010 article by a researcher with the Centre for Reproductive Biology of The Queen’s Medical Research Institute, Edinburgh, UK, who is author or coauthor of 303 studies, refers to the high incidence of low sperm counts in young (European) men and evidence for declining sperm counts in recent decades.103g   

 

Fig. 7.b

 

http://www.pollution-effects.info/index_files/image018.gif 

Development of the male sex glands, which have reportedly been increasingly malfunctioning in recent years, is apparently greatly affected by male hormones during infancy.  Testosterone normally increases very significantly in males during the early months after birth (see Figure 7.b here);103h this is normally accompanied by a high rate of testicular growth at that time. This rapid early testicular growth is followed by relatively little growth until 5 years of age.103k It is probable that proper development of male sex glands depends on the normal (that is, increased) supply of testosterone during those early months after birth.103m  Relevant to that, reduction of testosterone is known to be an effect of three different pollutants that are authoritatively recognized to be at high levels in breast milk; see below.  Bear in mind that breastfeeding rates had increased greatly in the 15 to 20 years leading up to the births of the young men who were later to have such diminished testosterone levels and semen quality. (See Figures 7 and 8.a)

 

 

 

 Section 7.b.1:  Effects of dioxins, which have been found to include reduction of testosterone levels as well as testicular atrophy; long-term deficits in male neurological development and motivation are likely outcomes.

 

 

According to a team of 13 researchers with the EPA, animal tests by at least two different research teams have indicated that dioxins were able to “impair testosterone synthesis,” among other effects.105   A CDC report accessed on the CDC website in April of 2016 says that dioxins have been demonstrated in studies of environmental and occupational exposures to have led to lowered testosterone levels in men; six studies were cited in support of that statement.  Further, it says that animal studies have demonstrated effects of dioxins including lowered testosterone levels and testicular atrophy.104 

 

With the above in mind, remember the findings that (a) at 11 months of age, dioxin toxicity-equivalent concentrations in breastfed infants had become about 10 times higher than in formula-fed infants;79 and (b) even at ages 18 to 26, average dioxin concentrations were found to be still twice as high in breastfed young men as in those who had been formula fed.77

 

Therefore there is ample reason to predict that long-term effects of breastfeeding could include reduction of hormones that are important to male motivation and attention.

………….

 

Continuing on the subject of factors that could specifically affect progress in education, remember from Section 3.c the study that found effects associated with common elevated levels of dioxins in a general human population:  learning disability and attention deficit disorder were found to be two and three times as high among children with common elevated levels of dioxins as among children with undetectable levels.80  That study did not investigate effects on males and females separately; but considering the above-indicated effects of dioxins in reducing the principal male hormone (testosterone), a hormone that is important to attention and neurological development, it is very likely that the education-related effects of dioxin would be found to be greater in males, if measured separately.

 

 

Section 7.b.2:  Effects of PCBs regarding testosterone, including far greater effects in adulthood than in childhood:

 

A 2010 study states that several studies have reported “inverse associations between PCBs and circulating testosterone levels in men.”106a  The study mentioned just below (published later) was in addition to the several earlier studies that had arrived at such findings.

 

A 2014 American study, by a team of six researchers who were authors or coauthors of over 160 studies among them, found that an increase of 10% in PCB levels in adolescent human males was associated with a 5.6% decline in their testosterone levels.106d  If PCB levels in adolescence seem to be only remotely related to breastfeeding exposures, there is actually a very significant relationship:  Duration of breastfeeding has been found to be a significant predictor of child PCB levels even at age 14;106e  30% higher PCB levels were found among breastfed than among non-breasted youths at age 10-17.106f

Fig. 7.b.1

PCBincrease_wBFing.gif 

Given that testosterone levels are significantly reduced in association with PCB levels, remember how far PCB levels can increase as a result of breastfeeding, depending on the duration of the breastfeeding (see this chart and Figure 4 as illustrations).  Remember that, in addition to its importance to motivation and attention in adolescence and beyond, testosterone is also important (during infancy) for neurological development and probably also for development of the testicles. (see Section 7.b, especially Figure 7.b) 

 

In a 2001 experiment with rats (Kaya et al.106c ), developmental exposure to PCBs was found to result in reduction of testosterone, but with noteworthy differences according to time period.  In the lowest-exposure group (which was the group with greatest similarity to typical human exposures), reduction in testosterone stemming from effects of exposure to PCBs during infancy rose from 12% in infancy to 34% in adulthood.  Normal development of the glands that produce testosterone in adulthood was probably disrupted by the exposure to PCBs during infancy.  

 

So it appears that the cognitive effects of developmental PCB exposures are likely to be so minor in young children as to go unnoticed, at that early stage.  This sheds some light on the studies that have not detected adverse effects of the high levels of PCBs in breastfed infants, on the basis of testing of young children.

 

But the ultimate effects of the developmental PCB exposure could become substantial in adolescence and adulthood; remember from earlier in Section 7.b that effects of reduced testosterone include reduced motivation and attention. 

 

Considering the above evidence of long-term effects of PCBs in reducing production of hormones that are important to male cognitive functioning, it may be worthwhile to remember the 2010 summary of studies indicating that PCBs had been found to be present in human milk in doses 63 to 270 times the minimal risk level established by the U.S. ATSDR;23 and that report should be seen in comparison with a study by U.S. scientists that found no detectable PCBs in all but one of 104 samples of infant formula.30

 

Also, the apparent destructive effect of developmental PCB exposure on male learning ability, as found in the Colciago study described in Section 7.a, may have been mediated by effects of PCBs on testosterone.

 

 

Section 7.b.3:  Effects of PBDEs that are relevant to progress in education:

 

Remember from the beginning of Section 7.b the importance of testosterone to male motivation and attention, then note the following quote from a study by a pair of scientists who are authors or coauthors of a total of 148 published studies:  "…most PBDEs have antiandrogenic activity….  Some PBDEs have been found to inhibit a key enzyme in the synthesis of testosterone…."107 More about effects of PBDEs, including in typical exposures, of substantially reducing testosterone can be found in part C.2 of Appendix C of this article.

 

According to a 2005 animal study, The exposure to low-dose PBDE-99 during development caused hyperactivity in the offspring…. The doses used in this study… are relevant to human exposure levels.108 (italics added)  

 

Considering the above, remember the evidence in Section 3.b about the effect of breastfeeding on a child’s PBDE levels, including the finding of a 2007 study that PBDEs were about five times higher in children who had been breastfed than in those who had been formula-fed even as late as age four.54

 

Section 7.b.4:  Estradiol, a hormone that is neurodevelopmentally important for both sexes, is also reduced by PCBs and PBDEs, and is reduced far more in males than in females.

 

The text and charts needed to explain the material summarized in this bold heading are somewhat lengthy, so they have been placed in Appendix E rather than taking up considerable space here. But the heading just above is an accurate summation of what could reasonably be concluded from what is presented in that Appendix.

 

 

Section 7.c:  The above toxins may well be the only developmental toxins that have been found to have adverse neurological effects distinctly on males.

 

Very substantial searches on both Pubmed and Google Scholar, searching for “toxins that affect male mental function,” brought up no studies that have found male-specific effects of any toxins other than the toxins dealt with above.

 

All of those toxins widely reach infants in high doses by way of breastfeeding, and are at extremely minimal levels or non-detectable in infant formula. (see Section 3)

   

 

Section 7.d:  There is close historical parallel of increases in breastfeeding with births of males who will later have problems associated with testicular dysfunction.

 

As indicated above in Section 7.b, considerable evidence indicates that toxins that are at high levels in human milk can lead to reduced testosterone, which in turn is very likely linked with broader testicular dysfunction, of kinds seen in Figure 8 below. Bear in mind the CDC report stating that dioxins have been found to lead to testicular atrophy.104  The probable effects of low testosterone that we are discussing here (low motivation, inattention, and more) are by no means limited to childhood.

 

­Fig. 8­                                                                                            Fig.  8.a

 

http://www.pollution-effects.info/index_files/image019.gif

Figure 8 above shows substantial decline in major aspects of testicular function in Finnish men born after 1979; such declines have apparently been common in western nations in recent decades (see the paragraph above Figure 6.b).  Some studies have seen signs of general declines in testicular function among men born before the 1970’s, but those findings have been strongly debated.112b

 

……………………..

 

 

Notice (in Figure 8.a just above and Figure 7 earlier) that activity of the major pathway for chemicals that are toxic to testicular function has increased dramatically in the U.S. and western Europe in recent decades; and during those same approximate years when breastfeeding was greatly increasing,

  a) large numbers of boys have been born who have had problems in education (see beginning of Section 7), and

  b) neurological disabilities, also, have greatly increased among American children, and those disabilities have been over twice as high among males as among females.112a . (see Figure 11 and Section 1)

 

 

 

 

 

Section 8:  Pesticide effects and comparative exposures of infants: 

 

 

Although pesticides have apparently not been officially designated as neurodevelopmental toxins, as was the case with the toxins discussed earlier, there are good reasons to believe that they should be so designated.  According to a European/American team of scientists, many pesticides used in agriculture target the nervous system of insect pests,”  which is of special concern because of the “similarity in brain biochemistry” between insects and humans.112c  A commission of the U.S. National Research Council (of the National Academies), in a report entitled, “Pesticides in the Diets of Infants and Children,” refers to “specific periods in development when toxicity can permanently alter the function of a system;” such periods of special vulnerability to toxins were said to apply to development of the central nervous system, which the commission says “may demonstrate particular sensitivity (to toxins) during the postnatal period.99v

 

 

Section 8.a:  Human milk has been found to normally contain many pesticides, and infant formula in the U.S. has been found to contain essentially none.

 

In a 2006 study in which breast milk samples from Denmark and Finland were examined, 13 different pesticide residues were detected in each of at least 90% of the 130 breast milk samples tested, in addition to other pesticides found less frequently.  The average concentrations were over 10 times the lowest concentrations measured, and there was no indication that the lowest levels measured were especially low.140  A 2011 study (Weldon et al.), investigating pesticides in breast milk samples from the urban Bay Area and a rural area in California, found detection rates of chemicals (mostly pesticides, but also PCBs and degradates of DDT) similar to the above; the authors noted that their findings for urban populations were very similar to those for agricultural populations, and attributed the urban exposure mainly to pesticides in foods.141 

 

See Section 8.b.3 below for much more information about how very substantial the pesticides in human milk are; and see Section 8.b.2 just below for evidence of strong adverse effects of those toxins on child development as a result of current levels of human background exposure.

 

Quoting from a publication of a commission of the U.S. National Academy of Sciences, measurements have consistently demonstrated that no pesticides are detected in finished infant formulas. These invariably negative analytical findings are attributable to ingredient selection and processing procedures that reduce the potential for pesticide residues to appear in the finished product.142 (italics added)  In 2013, the U.S. Department of Agriculture reported testing over 300 samples of infant formula and finding no detectable pesticide in 100% of dairy-based formula tested and in 99.4% of samples of soy-based formula that were tested.143

 

Section 8.b:  

Section 8.b.1:  Exposures of children to pesticides at current background levels correlate well with reduced mental capacities.

 

According to a 2012 article by Dr. David Bellinger, professor at the Harvard School of Public Health and author (contributing or primary) of over 250 published studies, the total loss of IQ points in American children associated with exposure to organophosphate pesticides alone is over twice as great as the total losses associated with ASD (autism spectrum disorders).138  Note that organophosphates are one major type of currently widely-used pesticides.  A study done for the European Union found similar loss of IQ points in the EU associated with exposures to organophosphates, as well as almost 60,000 cases of intellectual disability annually in the EU, at total cost of about 146 billion Euros per year (over $160 billion);138b the authors' focus was on damage to the developing brain by widespread environmental chemicals during the period spanning fetal development through puberty.

 

 

Organochlorine pesticides, including DDT, have by now been banned for most uses in most developed countries, but their continued use (for malaria control as well as agriculture) in developing countries means that they are widely present not only in those countries but also in a high percentage of fruits, vegetables, farm-raised seafood, and other popular food consumed in developed countries, since much of that food is imported. 137a, 137c

  

Considering the continuing widespread exposures to organochlorine pesticides (including DDT), the following results from a 2002 study should be of considerable interest:  Average DDT levels were measured in mothers at time of birth in various geographic areas (10 countries and 14 German states); 15 years later, higher average time-of-birth DDT levels correlated well with lower average mental capacities in school-age children in those same locations.  (see chart below)   

Fig. 9

 

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 The possibility that the correlation was mainly related to prenatal exposures should be considered. But prenatal exposures to most such toxins are small (due to the effect of the placental barrier) compared with postnatal exposures via breastfeeding;17  the postnatal period is one of continued high vulnerability, and often higher-than-prenatal vulnerability, to effects of toxins. (see Section 2 above)  

 

Fig. 9a

DDTexcesses.gif

Notice in the bottom line of data above, showing data for Total DDT as found in studies carried out in South Africa, that the mean (average) level of DDT residues in bovine milk was found to be less than a quarter of the maximum residue limit (MRL) for bovine milk; on the other hand, mean breast milk levels of DDT were found to be 15 times that same MRL137b

  

 

Section 8.b.2:   Pesticides associated with ASD, ADHD, and other neurodevelopmental problems:

 

For information about close links between ASD and pesticides, including pesticides transferred via lactation, see Section 4.a.2.

 

In a 2010 study it was found that, for the most commonly detected metabolite of organophosphate pesticides, children with levels higher than the median of detectable concentrations had twice the odds of ADHD compared with those with non-detectable levels.137e Note that this doubled risk of ADHD applied to 50% of the child population that had detectable concentrations of the pesticide; bear in mind that many pesticides have been detected in the breast milk of each of 90% of women in studies, mostly in concentrations many times the limit of detection;140, 141 the above study's finding implies that a large part of the child population in general appears to be at risk for ADHD as a result of very typical exposure to pesticides.

 

Given the above, remember (from Section 8.a) the authoritatively-determined high levels of pesticides in human milk and the near absence of them in infant formula; those are the two main alternative feedings ingested during the early postnatal period when the brain’s development is highly vulnerable to toxins. (see Section 9.b)

 

 

Section 8.b.3:  There are many reasons to see breast milk as being by far the predominant source of pesticide exposures to infants during the early-postnatal period of rapid brain development.  A partial listing of evidence, in addition to that already presented in Section 8.a, follows:

 

--  According to a commission of the National Research Council of the U.S. National Academies, "the gastrointestinal tract is the major portal of entry of pesticides into the body."139b 

-- Concentrations of DDT and some PCBs were found to be ten times as high in breastfed infants as in bottle-fed infants after six months of breastfeeding, in a 2005 study in Germany;139c

 

--- Organochlorine concentrations (including metabolites of DDT, which is the best-known organochlhorine) were found to be still four times as high in breastfed infants as in bottle-fed infants at age four, and still over twice as high at age 14, in a 2015 study in a western country (Spain) in which DDT was banned in 1977.139d

 

-- A relevant statement was made in 2006 by two leading experts on toxins involved in child development, P. Grandjean and P.J. Landrigan, each of whom are first or contributing authors of hundreds of scientific studies; they reported that 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.139e

 

-- Infants would not normally be at the stage of hand-to-mouth activity until after 6 months of age,98g6 which means that infant exposures from surroundings would usually be minimal during what is likely to be the most sensitive period of postnatal development. (See Section 2)

 

Remember from the Bellinger and EU statements earlier that the organophosphate type of pesticides alone has been associated with massive loss of IQ points and tens of thousands of cases of mental handicap every year.  That is not even counting the effects of the many other kinds of pesticides, which are generally considered to also be neurologically toxic.

 

 

Section 8.c:  Adverse effects of pesticides specifically on males.

Remember from Section 7 about the unexplained very high ratios of males to females among children affected by the increasing neurological disorders (especially ASD and ADHD), as well as the disproportionate cognitive deficiencies of young males in the general population in recent years.  In addition to the studies included in the Rossignol et al. review in Section 8.b (it came later), was a 2016 Chinese study that found postnatal exposures of human children to typical contemporary (organophosphorous) pesticides to have adverse sex-specific neurological effects as follows:  The odds ratios for developmental delay in the motor area of boys with higher concentrations of DE and DAP pesticide metabolites were 264 to 1 and 145 to 1. The adverse effect of postnatal concentrations of DE on the social area of boys was in a ratio of 57 to 1.99t

 

Regarding the air pollutants that were found (in the Rossignol review discussed above) to be the other category of toxins most associated with ASD, bear in mind that

a) the specific type of air pollution that was most frequently found to be associated with ASD was emissions from vehicle traffic, and

b) PCBs, PBDEs and dioxins are all developmental toxins that are components of vehicle emissions,99u and those toxins all become concentrated in human milk -- see Sections 3.a, 3.b and 3.c above.

 

 

 

 

Section 9:  

 

The time when toxic exposures take place is critical in determining their effects; vulnerability is greatest when development is active. (see Section 2).

 

 

  Fig. 11

 

image031.gif

 

Those early months are the vulnerable developmental period for the functions that have become so increasingly impaired.

  

Breastfeeding, transferring six different developmental toxins to infants, each in very significant amounts (see Sections 3 and 8)  is by far most prevalent during the early months after birth;99x also, the concentrations of some of those toxins are apparently much higher during earlier breastfeeding. (see "Early higher exposures" near the beginnings of each of Sections 3.a, 3.c and 3.d)  The combination of the above, together with breastfeeding's effect of concentrating toxins (see Section 2.b), leads to far greater total transfers of toxins soon after birth than at any other stage of development.

 

The feeding type that is at the base of those high early-postnatal transfers went through major increases in the late 20th century, in the U.S. and many other countries. (see Figures  7 and 8.a

 

Could there be a connection between (a) the very large increases that have occurred in infants' toxic exposures that take place during the early-postnatal period (see just above) and (b) the unexplained major increases in impairments in functions that are especially vulnerable to toxins during the early postnatal period?

 

............

 

There might be other toxins or sources of toxins that have also greatly increased in the environment during the period when the disabilities have increased greatly, but breastfeeding as a pathway for developmental toxins is distinctive and possibly unique in several important respects:

   a) four toxins in breast milk widely reach infants in doses well in excess of recognized safe levels (see Section 3).  s

Substantial inquiry about existence of any other toxins to which infants are recognized to be widely exposed in excessive doses, in letters addressed to organizations and scientists with appropriate expertise, has had only one result:  none of the several replies that were received suggested any.other toxins that might qualify in that respect. (See Section 6)  The principal alternative infant food contains very little or none of those toxins. (see Section 3)

 

   b) Some of the toxins in breast milk have been found to affect males predominantly, which makes a very good fit with the otherwise unexplained disproportionately-high percentage of males affected by autism and ADHD; (see Section 7)

 

   c) several studies have found breastfeeding duration to be positively correlated with prevalence of autism, including in dose-response relationships; (see Section 4) and

 

   d) Breast milk is a predominant or sole source of food for most infants during the especially sensitive early months after birth; (see Section 2.d and Section 9.b just below about special vulnerability of development during those early months).  This means that exposures to toxins in the milk during that very vulnerable period are intensive in a way that could probably not be equaled by normal exposures to any other toxins; remember the Chien et al. study that found that over 95% of breastfed infants' exposures to mercury came from breastfeeding.96

 

..............................................

 

 

Section 9.b: In those same early-postnatal months, other neurological development is also taking place that has not been going well during the period of major increases in early-postnatal transfers of toxins to infants:

 

The first three months after birth are the period in which growth of connections in the prefrontal cortex is especially rapid;114f bearing in mind that development is especially vulnerable to effects of toxins while the development is active (see Section 2.a), those first months are therefore the time when normal formation of that brain region is unusually vulnerable to effects of environmental toxins.  The following areas are controlled or strongly affected by the prefrontal cortex:

--  sustained attention,

--  formation and retrieval of memory,

--  aspects of intelligence, including ability to formulate and carry out behavioral plans,

--  speech,

--  gaze control; 114g

--  comprehension,

--  perception114j

 

It should be apparent from the above list that defects in development of the prefrontal cortex could be highly relevant to (a) ADHD (sustained attention), (b) learning disability (memory, perception, and comprehension), and (c) ASD (all of the above, with gaze control/eye contact being especially distinctive as a problem in those with ASD). 

 

That means that exposure of an infant to neurodevelopmental toxins during the first three months after birth, when connections are forming rapidly in the prefrontal cortex, could be of especially great significance regarding those increasingly-diagnosed disorders.  

  

.......................................

 

According to a leading authority on development of the brain,114e there are other specific areas of neurological development that are known to take place in the first six months after birth, which will be listed below; most of those are areas in which there have also been strong indications of faltering development in recent decades, especially in males.  Those include the following:

-- behavioral indices of attention;

(deficits in attention are clearly central to ADHD, which has greatly increased in recent decades; and attention problems are also a frequent trait of autism)

-- behavior in response to novel stressors;

(inappropriate, agitated responses to novel situations or stimuli are well known to often be traits of those with the increasingly-diagnosed ASD)

-- circadian rhythm;

(this ties in with the frequent problem of children with autism not wanting to sleep at night)

-- the motor system;

(clumsiness is a frequent trait of those with ASD)

 

As common durations of breastfeeding increased to six months and more during the most recent decades (see Figure 7), the above areas of neurological development would have been receiving increased exposures to the developmental toxins that are known to be high in breast milk (see Section 3).

 

 

For additional information about special sensitivity to neurodevelopmental harm during the early months after birth, see Section 2.d.

 

………………………..

 

 

Section 10:  A reasonable question to consider:

(Some of the following is the same as the final part of the introductory summary, but it is worth repeating now that the information leading up to and supporting it has been presented.)

 

The above brings us to some important matters to think about:

 

Considering that

  (a) non-communicable disorders have been greatly increasing among children in recent decades -- for basically unknown reasons (Section 1),

  (b) the developmental processes taking place after birth are authoritatively recognized to be vulnerable to toxins ingested postnatally (Section 2),

  (c) toxins known to be typically at high levels in human milk have been found to lead to effects similar to symptoms of the increasing disorders (Section 3); and breastfeeding has been increasing while the disorders have been increasing (Figures 7 and 8a), and

  (d) positive dose-response relationships have been found between breastfeeding and autism, in several published studies (Section 4),

 

it is reasonable to ask the following question of the medical organizations that promote breastfeeding:

 

How has it been determined that developmental toxins in human milk have not been contributing to increases in disorders that could outweigh the benefits of breastfeeding?

 

 

The U.S. medical associations that promote breastfeeding (pediatricians, family physicians and obstetricians and gynecologists) do not respond after being repeatedly asked the above question (with variations in the wording).

 

Since there is substantial peer-reviewed scientific evidence to support (a) through (d) above, it would seem to be appropriate for those physicians’ organizations to consider that evidence before they recommend feeding infants a food that has been authoritatively determined to contain developmental toxins in concentrations far exceeding established safe levels. That would be especially called-for given that child neurological disorders have increased in parallel with the major increases in breastfeeding. (see Sections 1 and 5.)  And a response to the above question would be even more in order considering the apparent absence of widespread exposure of infants, by any pathway other than breastfeeding, to developmental toxins in doses exceeding established safe levels (see Section 6).

 

If careful study had been carried out on such an important matter of public health, a written record of the analysis of the important evidence ought to be available to the public. But there is apparently no such record, which implies that the breastfeeding recommendations are based on something other than careful consideration of the important evidence. Doctors, like the rest of us, are subject to groupthink and other conformity-inducing social influences, and there can be no doubt that there is a powerful popular movement in favor of breastfeeding.

 

The apparently unmet need for careful consideration of scientific evidence on both sides of this topic is especially great since there is an alternative feeding that worked well for an entire generation born in the mid-20th century U.S., before the generations were born that have had major increases in non-communicable disorders. (see below)

 

 

A 2008 study found that 78% of women would stop breastfeeding if they were aware of just one toxin in their milk, even at low levels.132  Most American mothers do breastfeed, indicating that most of them are not aware of the presence of any of the toxins in their milk, not to mention four toxins, each present in high concentrations, plus two others in very significant concentrations, all of which are either low or absent in U.S. infant formula, according to authoritative assessments.

 

There is considerable case law that applies to a parent’s right to be informed about toxins contained in breast milk. According to a decision of the Supreme Court of Washington (state), citing two earlier cases, “Important decisions must frequently be made in many nontreatment situations in which medical care is given….The physician's duty is to tell the patient what he or she needs to know in order to make them” (the decisions).133  (A doctor’s advice about infant feeding clearly influences an important health-related decision.)  The Supreme Court of Wisconsin stated in 2012, "a growing number of courts require physicians to disclose what a reasonable person in the patient's position would want to know."133a (emphasis added)  As of 2016, courts in the U.K. and in half of U.S. states had adopted such a standard.133b  As indicated in the above-cited study,132 verifying what should be intuitive, most women do consider knowledge of presence of toxins in breast milk to be a crucial determinant of their decisions about whether to breastfeed.  Doctors therefore apparently have a legal obligation to tell mothers about those toxins, as part of consultations on breastfeeding.

 

For additional information about doctors’ legal obligations to inform parents about toxins contained in breast milk, see www.medical-liability.us

 

Note that an alternative type of infant feeding is readily available that

 

(a) compared with human milk, contains less than 7% (and usually less than 1%) as much of the developmental toxins mentioned (see near the beginning of each of the subsections of Section 3), and

 

(b) was the standard feeding type for the entire generation born in the U.S. “throughout the mid-20th century,” as stated by the American Academy of Family Physicians.134  According to what appears to be the most thorough study of infant feeding patterns in the U.S., breastfeeding declined until 1960, and “since the middle 1960s there has been a steady increase in the practice of breastfeeding in the US.”134a  This is compatible with the historical chart (in Figure 7) provided by another authority on the history of breastfeeding. Remember that childhood disabilities and disorders, which by now have reached high levels, were reported to have first started emerging as major chronic conditions in the 1960’s, followed by more substantial increases beginning in the 1970’s and later (see Section 1). Even flat breastfeeding rates (in 1962-1965, following earlier declines -- see Figure 7) would have been instrumental in an increasing transfer of developmental toxins to infants, considering that an increase of toxins in human milk had already begun approximately during the 1950’s.22

The generation that was seldom breastfed did not have childhood health problems on the scale that was to become commonplace after breastfeeding rates increased greatly. Evidence to support that statement (in addition to what was already presented in Section 1) includes the following: 

 

According to a 2007 article in the Journal of the American Medical Association, “the number of children and youth in the United States with chronic health conditions…has increased dramatically in the past 4 decades.” The authors referred to various studies finding very large increases in obesity (almost quadrupling in U.S. children between the early 1970’s and 2004), disability associated with childhood asthma (tripling between 1969 and the mid-1990s), and activity limitations due to a health condition of more than 3 months’ duration (quadrupling between 1960 and 2004). The authors predicted that “the expanding epidemics of child and adolescent chronic health conditions will likely lead to major increases in disability among young and then older adults in the next several decades.144

 

Studies in the New England Journal of Medicine and the Journal of Allergy and Clinical Immunology point to the 1970’s as the beginning of doubling and tripling of allergy rates, especially among children and young people.145  There is also ample evidence pointing to the 1970’s as the time when major increases in childhood diabetes began.146 Evidence also indicates that ADHD grew from very low to over 14% of U.S. boys over age 7 during the last few decades.147

 

Apparently, all of this serious health decline occurred among children born after the mid-20th-century births of the generation that was seldom breastfed.

 

…………………………

 

Authoritatively recognized low quality of the kind of studies that have found benefits of breastfeeding, compared with randomized trials that have found very different results

 

Essentially all of the studies that have found benefits of breastfeeding have been observational studies, according to former U.S. Surgeon General Regina Benjamin.a1a  The leading authorities on medical evidence have determined that evidence from observational studies is predominantly of low quality, with only exceptional ones reaching a medium level of quality. One such determination has been provided by Dr. Gordon Guyatt and an international team of 14 associates;a2 Dr. Guyatt is chief editor of the American Medical Association’s Manual for Evidence-based Clinical Practice, in which 26 pages are devoted to examples of studies (most of which were observational) that were later refuted by high-quality studies.a2a  A similar assessment of the low quality of evidence from observational studies has been provided by the other chief authority on medical evidence (Dr. David Sackett),a2c  writing about “the disastrous inadequacy of lesser evidence,” in reference to findings from observational studies.a2b

 

When people choose or  don't choose an intervention, such as breastfeeding, that introduces "confounding" due to different types of people choosing one or the other alternative; specifically, mothers of higher socio-economic status (with better health-related circumstances) and people who adhere to medical guidelines (who also have better health habits in general) are much more likely to breastfeed, causing confounding as to what are the real causes of the outcomes;  better child health is found to be associated with breastfeeding and conclusions are typically drawn on the basis of those associations; but the associations could well be because of the confounders.  Researchers typically claim to adjust or control for the confounding, but there is no way to measure such things accurately, so adjustments are normally insufficient.

 

Randomized studies, although still subject to biases, are recognized to provide far superior evidence compared with observational studies, since the treatment is randomly assigned rather than chosen.  It is considered to be improper to dictate to mothers whether or not they should breastfeed, so there have been no truly randomized studies of breastfeeding versus formula feeding.  (The studies in Belarus had randomized promotion, but the mothers still chose to breastfeed or not.)  But there have been two randomized studies at the edges of the breastfeeding-versus-formula question, which have been revealing:

 

image032.gifA study was conducted of effects of alternative feedings of preterm infants, in which the infants were randomly assigned to be fed either banked human milk or a combination of human milk and infant formula, as supplements to the mothers' milk.  As seen in this chart, developmental quotient scores (at nine months) of infants fed partially with formula did better than infants fed with banked human milk.  The higher scores for partially-formula-fed infants also applied in all of the six subgroups that were studied:  boys, girls, babies ventilated for less than or more than 24 hours, and sizes appropriate for or small for gestational age.  The authors noted that "it was surprising that a brief period of dietary manipulation (median 30 days) could have such prolonged consequences."147a

 

 

 

The next chart is also from a randomized trial, one that shows results that are in sharp conflict with the usual observational studies that have found benefits of breastfeeding.

 

 

Figure 12

Below:  Prevalences of various allergies, with and without exclusive breastfeeding

 

   

 

Title: prevalence of allergies in relation to breastfeeding - Description: Allergies have been  found to increase greatly among infants who are exclusively breastfed, compared with those who were fed common allergenic foods early, including peanut, egg, milk, fish, semame and wheat.
 
 

One could search in vain for any reference to this study, or to other studies negative to breastfeeding (such as in Section 4), in the Policy Statement on breastfeeding of the American Academy of Pediatrics. 146a  But one could find ample reference to "the protective effect of exclusive breastfeeding” in that AAP statement, including in the section on allergies.  

 

Bear in mind the doubling and tripling of allergy rates that have occurred in recent decades, especially among children and young people,145 while breastfeeding rates have increased at least that much.

 

In addition to randomized studies, another type of study that is an improvement over the usual observational studies is indicated by the EPA as follows:  Epidemiologic studies of exposed human populations provide the most convincing evidence of human health effects.”145a For results of an epidemiological study that found positive correlations between breastfeeding and autism, and between more extended breastfeeding and greater prevalence of autism, based on data from all 50 U.S. states and 51 U.S. counties, see Section 4.

 

 

Related to the effects of shielding developing infants from allergenic foods, discussed above, also note the following:

 

Breastfeeding also protects infants from bacterial challenges,

 

by means of the antibodies in human milk; and again there is good evidence indicating that the eventual outcomes of the protection have turned out to be adverse rather than favorable.

 

While developing infants were receiving greater shielding from bacteria by means of increasing breastfeeding (late 1960's to present), auto-immune and allergic diseases among children increased greatly. 146 (as did many other diseases -- see "Additional evidence" above). Decline in immunity in relation to increased shielding is in line with the highly-regarded hygiene hypothesis. According to that hypothesis, reduced exposure to common infections leads to increases in those disorders, presumably because of lack of challenges that would otherwise be stimulating the development of the immune system.  Included among the increasing auto-immune and allergic diseases is asthma, which increased sufficiently during the decades when breastfeeding rates were greatly increasing that it came to be referred to as an epidemic.149  Type 2 diabetes, also, was authoritatively declared to have become an epidemic, principally among children and young people, as of 2002.150  There have been remarkable parallels between highs and lows of childhood diabetes prevalence and highs and lows of breastfeeding rates geographically and according to time -- see www.breastfeeding-and-diabetes.info. 

………………..

 

 

 

It appears that well-meaning people have built up a powerful bandwagon on the basis of what seemed to make sense, based on what was known at an earlier time. They found that their ideas could be confirmed by studies; but those studies were very much subject to confounding by underlying other factors.  It is normal in studies to attempt to control or to make adjustments when trying to minimize effects of confounders; but according to a 2014 study by a team of eight researchers, "it is generally considered impossible to completely mitigate the potential for bias associated with observational studies through study design or analytic method because residual unidentified confounding factors can rarely be ruled out, and statistical adjustment or matching procedures are often inadequate."150a  Remember from the discussion of "observational studies" (earlier in this section) that essentially all studies that have found benefits of breastfeeding are of that type, a type that leading authorities on medical evidence consider to be basically of low quality.

 

One confounder that would especially apply to breastfeeding studies is the "adherer effect," which recognizes that people who faithfully follow medical instructions are different from those who don't; the presumed relevant difference is that people who follow medical instructions diligently are better at following guidelines for good health in general, leading to health benefits completely aside from effects of any particular therapy that is being tested.  There can be no doubt that "adherers" among mothers would be very predominantly breastfeeders, considering the strong promotion of breastfeeding that comes from the medical community150b as well as from many seemingly-informed private citizens. 

 

The adherer (or "compliance") effect stood out in the case of hormone replacement therapy (HRT).  This therapy was found in various large observational studies to be beneficial for women who faithfully complied with it. As of the mid-1990s, the American Heart Association, the American College of Physicians, and the American College of Obstetricians and Gynecologists had all concluded that the beneficial effects of HRT were sufficiently well established that it could be recommended to older women as a means of warding off heart disease and osteoporosis.152   When results came in from randomized studies, the study type recognized to be of high quality, it was found that outcomes of the HRT therapy were actually worse rather than better, in women who went through that therapy.  According to a New York Times article, quoting Dr. Jerome Avorn, a Harvard epidemiologist, the observational studies may have inadvertently focused their attention specifically on the “Girl Scouts in the group, the compliant ongoing users, who are probably doing a lot of other preventive things as well.”152  Defenders of observational studies say that they can control or adjust for confounders, but according to Rory Collins, an epidemiologist at Oxford University, “you can’t measure these things with precision so you will tend to under-correct for them. And you can’t correct for things that you can’t measure.” 152  There are good reasons why the leading authorities on medical evidence have such a low opinion of observational studies. (see earlier)

 

Figure 12.1 (source of chart at ref. 151)

People who faithfully follow medical instructions (such as the recommendations to breastfeed) are different from those who don't; their health-related habits are better.  Their health -- and probably the health of their children -- is also likely to be better, even if the related recommendation is useless.

 

image042.gif
 

Good adherence to recommendations --- even to placebo — is associated with better health outcomes.

 

In addition to the meta-analysis of studies summarized in the above chart, other studies have arrived at similar findings, of favorable health outcomes among those who diligently follow health instructions, even if the instructions are to take medically ineffectual sugar pills.151, 151a  A 2014 study by a ten-scientist team broadened the range of observed relevance of the adherer effect, in randomized trials with placebos, finding "a strong and significant inverse association between adherence to placebo and hip fracture, CHD, invasive breast cancer, cancer death, and all-cause mortality" in women.153

 

The authors of the Simpson study (a chart from which is shown above), when summarizing their review of other studies, stated, "For participants with good adherence to placebo or beneficial drug therapy, the risk of mortality was about half  that of participants with poor adherence."  Their assumed explanation was that "the presence of good adherence is a marker for overall healthy behaviour."151  Specific aspects of healthy behavior would include diet, exercise, regular follow-up with healthcare professionals, immunizations, and screenings, all of which would also provide health benefits to an infant under an adhering mother's care.

 

A 2014 study cites three other studies from 2005 and later (in addition to the studies mentioned above) in support of its statement, "A growing body of evidence suggests that good adherence to treatment is an important predictor of positive treatment outcomes, regardless of whether the treatment is an active therapy or an inert placebo."  And also, "The fact that good adherence among the placebo group is beneficial across a variety of medication trials, health outcomes, and patient samples suggests that this is a robust and reliable effect."154

 

The adherer effect overlaps with effects of socioeconomic differences.  According to data provided by the U.S. Surgeon General, college graduates appear to be about twice as likely to breastfeed for six months or more as high school graduates.2  Mothers of lower socioeconomic status are much more likely to smoke (which is a health risk factor for nearby infants3) and "to eat what’s affordable rather than what the experts tell them is healthful, to have poor medical care and to live in environments with more pollutants, noise and stress;"152 such characteristics would obviously carry over to adverse health effects on infants of the non-breastfeeding mothers who are disproportionately of lower income and education.  Conversely, health advantages are normal at the higher socio-economic levels, a common position of the families in which a high percentage of mothers breastfeed; see "observational studies" earlier in this section.

 

More about the importance of considering long-term effects, which are normally ignored in discussion of effects of breastfeeding:

 

There is another lesson to be learned from the case of hormone replacement therapy, which Dr. Avorn (quoted earlier) refers to as the "estrogen debacle" (tens of thousands of deaths may have resulted from HRT152).  That lesson is the consequences of drawing conclusions from short-term outcomes.  It was long-term studies that eventually found the adverse outcomes of HRT, after short-term evidence had seemed thoroughly convincing to so many doctors and prestigious organizations.  That pattern has considerable relevance to breastfeeding; it appears that the vast majority of the studies that have found benefits of breastfeeding have drawn their observations to a close after early childhood.  But the toxins in breast milk are known to have principally long-term effects. (see Section 3.a.2)

 

Remember from Section 3.a.2 that effects of toxins, such as those found in human milk in concentrations exceeding established safe levels, have been detected well past early childhood, often only past early childhood.  Many studies were cited there, finding long-term effects of these toxins related to IQ and general mental capacities, motor development, male hormones (which are related to neurological development and function), and school performance, with the effects sometimes found to increase with age.  EPA scientists refer to “long-latency delayed neurotoxicity” when discussing effects of toxins such as are contained in human milk and that are minimal or absent in infant formula, and similar statements have been made by the U.S. ATSDR, WHO, and a commission of the U.S. National Academy of Sciences.  Additional evidence of long-term adverse effects of these chemicals (that are high in human milk) came from animal studies, including findings of effects that became apparent late and that worsened with age.  (Details and citations of sources for all of the above in Section 3.a.2)

 

The U.S. Surgeon General's Call to Action to Support Breastfeeding 2011makes only brief reference to long-term effects of breastfeeding (p. 1 at a1a), but what that document says on this topic is revealing if one looks at it closely.  After referring to short-term effects of breastfeeding (as found in observational studies), the document goes on to discuss associations of breastfeeding with longer-term effects, as found in a report on the subject, as follows:

 "The AHRQ report also concludes that formula feeding is associated with higher risks for major chronic diseases and conditions, such as type 2 diabetes, asthma, and childhood obesity, all three of which have increased among U.S. children over time."  Again, observational studies were the bases for the "risks" associated with formula feeding; it is quite reasonable that the Surgeon General suggests consideration of other relevant evidence, such as trends of increases in diseases in relation to exposures to possible risk factors present in the environment while those increases were taking place.  The Surgeon General's document does not go into any details regarding the trends, so we will do so here:

 

image046.gifFirst, we need to remember the time trend of breastfeeding in the U.S., rapidly increasing for a decade after 1972, then settling back and later continuing with slower increases.

 

 Furthermore, the risk of sudden infant death syndrome is 56 percent higher among infants who are never breastfed."  " The risk associated with some relatively rare but serious infections and diseases, such as severe lower respiratory infections and leukemia are also higher for formula-fed infants.

 

 

the risk of sudden infant death syndrome is 56 percent higher among

infants who are never breastfed

 

 

 

The American Academy of Pediatrics, despite the very ample evidence of developmental toxins in average human milk (see earlier and later in Section 3), does not mention environmental toxins even once in its policy statement, "Breastfeeding and the Use of Human Milk."37b  One might wonder whether the phrase, "the whole truth," has any meaning to some people when they are comfortably sitting on a bandwagon.  Such telling of half-truths would be excusable if parents were generally aware of the important information that is being withheld, but that is certainly not the case here.

 

Between the adherer effect and the fact that most breastfeeding studies have paid no attention to long-term adverse effects, it should not be surprising that many studies have found benefits of breastfeeding.  What should be surprising is that, despite the above, over 50 peer-reviewed studies have found overall adverse health effects of breastfeeding. (see www.breastfeeding-studies.info)

 

 

……………………………

 

For additional information about trends in health of American children since 1970, see www.breastfeeding-health-effects.info

 

For additional information about the toxins that have been found in human milk versus those in infant formula, see www.breastfeeding-vs-formula.info. 

 

Research needs:

In the U.S. CDC's publication, GUIDELINES FOR THE IDENTIFICATION AND MANAGEMENT OF LEAD EXPOSURE IN PREGNANT AND LACTATING WOMEN, the "Research needs" section near the end expresses a need for "development of new therapeutic agents or mechanisms to remove lead from breast milk." 98g3

 

That is certainly a sensible objective; but, considering the ample evidence of presence of other developmental toxins that are also present in human milk, in most cases in concentrations far exceeding established safe levels (see Section 3), a proper list of research needs should also include the following:

 

Development of means to remove PCBs from breast milk

Development of means to remove PBDEs from breast milk

Development of means to remove dioxins from breast milk

Development of means to remove mercury from breast milk

Development of means to remove pesticides from breast milk

 

Seeing such a list and considering the difficulties that would be involved in achieving more than minor reductions in levels of those toxins in the near or medium term, one might well become discouraged.  If so, it would be good to bear in mind that there is an alternative infant feeding that has very little or none of those toxins; and it is a feeding type that apparently worked well for the generation born in the mid-20th-century U.S., a generation that did not have the major increases in non-communicable diseases that have become commonplace among children since breastfeeding became widespread.  It should not be surprising that a far better history of child health prevailed during the period when formula-feeding was the norm, considering the known lack of developmental toxins in recognized excessive doses in that feeding type, as opposed to in human milk. (see Section 3)

 

 

Comments on the above are invited, including criticisms if they are specific, and will usually receive a response.  You can see our “Comments” section at www.pollutionaction.org/comments.htm.  In criticisms, please point out any specific passages that you feel are not accurately based on authoritative sources (as cited) or that do not logically follow from the evidence presented.  Note that the author of this article feels no obligation to present the pro-breastfeeding case as long as the medical associations and other promoters of breastfeeding fail to inform parents about the developmental toxins that are, without dispute, present in high concentrations in human milk. Please e-mail to dm@pollutionaction.org

 

 

About the author:

As the author of the above, my role has not been to carry out original research, but instead it has been to read through very large amounts of scientific research that has already been completed on the subjects of environmental toxins and infant development, and then to summarize the relevant findings; my aim has been to put this information into a form that enables readers to make better-informed decisions related to these matters.  The original research articles and government reports on this subject (my sources) are extremely numerous, often very lengthy, and are usually written in a form and stored in locations such that the general public is normally unable to learn from them. 

 

My main qualification for writing these publications is ability to find and pull together large amounts of scientific evidence from authoritative sources and to condense the most significant parts into a form that is reasonably understandable to the general public and also sufficiently accurate as to be useful to interested professionals. My educational background included challenging courses in biology and chemistry in which I did very well, but at least as important has been an ability to correctly summarize in plain English large amounts of scientific material.  I scored in the top one percent in standardized tests in high school, graduated cum laude from Oberlin College, and stood in the top third of my class at Harvard Business School.  

 

There were important aspects of the business school case-study method that have been helpful in making my work more useful than much or most of what has been written on this subject, as follows:   After carefully studying large amounts of printed matter on a subject, one is expected to come up with well-considered recommendations that can be defended against criticisms from all directions.  The expected criticisms ingrain the habits of (a) maintaining accuracy in what one says, and (b) not making recommendations unless one can support them with good evidence and logical reasoning.  Established policies receive little respect if they can’t be well supported as part of a free give-and-take of conflicting evidence and reasoning.  That approach is especially relevant to the position statements on breastfeeding of the American Academy of Pediatrics and the American Academy of Family Physicians, which statements cite only evidence that has been

   (a) selected, while in no way acknowledging the considerable contrary evidence,a1 and

   (b) of a kind that has been authoritatively determined to be of low quality. (See the paragraphs dealing with observational studies near the end of Section 10 above.)

 

When a brief summary of material that conflicts with their breastfeeding positions is repeatedly presented to the physicians’ associations, along with a question or two about the basis for their breastfeeding recommendations, those associations never respond.  That says a great deal about how well their positions on breastfeeding can stand up to scrutiny.

 

The credibility of the contents of the above article is based on the authoritative sources that are referred to in the footnotes:  The sources are mainly U.S. government health-related agencies and reputable academic researchers (typically highly-published authors) writing in peer-reviewed journals; those sources are essentially always referred to in footnotes that follow anything that is said in the text that is not common knowledge.  In most cases a link is provided that allows easy referral to the original source(s) of the information.  If there is not a working link, you can normally use your cursor to select a non-working link or the title of the document, then copy it (control - c usually does that), then “paste” it (control - v) into an open slot at the top of your browser, for taking you to the website where the original, authoritative source of the information can be found.  

 

The reader is strongly encouraged to check the source(s) regarding anything he or she reads here that seems to be questionable, and to notify me of anything said in the text that does not seem to accurately represent what was said by the original source.  Write to dm@pollutionaction.org.  I will quickly correct anything found to be inaccurate.

 

For a more complete statement about the author and Pollution Action, please go to www.pollutionaction.org

 

Don Meulenberg

Pollution Action

Fredericksburg, VA, USA

__________________

a1) See www.breastfeeding-studies.info and www.breastfeeding-toxins.info/

a1a) The Surgeon General’s Call to Action to Support Breastfeeding 2011, p. 33, at www.surgeongeneral.gov/library/calls/breastfeeding/calltoactiontosupportbreastfeeding.pdf

 

a2) Figure 2 in Guyatt et al., GRADE guidelines:  1. Introduction -- GRADE evidence profiles and summary of findings tables, Journal of Clinical Epidemiology, at http://www.jclinepi.com/article/S0895-4356(10)00330-6/pdf

a2a) Dr. Gordon Guyatt is chief editor of User’s Guides to the Medical Literature:  A Manual for Evidence-based Clinical Practice, 2nd Edition (3rd is upcoming), copyright  American Medical Association, published by McGraw Hill.

a2b) Writing in The Canadian Medical Association Journal, as quoted in “Do We Really Know What Makes Us Healthy?” New York Times, published: September 16, 2007  at http://www.nytimes.com/2007/09/16/magazine/16epidemiology-t.html?pagewanted=2&_r=0

a2c) In a review in the Journal of the Medical Library Association, only two guides are recommended for use by physicians in evaluating evidence in medical literature, one of which is the one edited by Guyatt et al., already referred to, and the other of which is by Dr. Sackett. (Journal of the Medical Library Association, Oct. 2002, User’s Guide to the Medical Literature:  A Manual for Evidence-Based Clinical Practice, Review by Rebecca Graves, at httpi://www.ncbi.nlm.nih.gov/pmc/articles/PMC128970)

 

 

 

Appendix B:  Please go to www.pollution-effects.info/appendixBandC.htm

Appendix C:  Please go to http://www.pollution-effects.info/appendixC.htm

Appendix D:  Another reason why learning disability can be seen to be linked with auditory harm associated with the early, most active months of breastfeeding:

 

Remember the effectiveness of breastfeeding in transferring PCBs to infants (see Figure 4), as well as the apparent effects of PCBs on hearing function.31, 30a  Bear in mind that normal hearing tests (assessing ability to hear beeps of sound) would not detect inability to understand meanings of sounds; and remember from Section 3.a that PCB exposures via lactation (at levels similar to some human exposures) were found to lead to “dramatically altered organization of the representations of sound” in the brains of half of the rats tested. Most children with learning disabilities have their primary deficits in basic reading skills, and research indicates that “disability in basic reading skills is primarily caused by deficits in phonological awareness”114c (phonological means related to speech sounds).  A child’s awareness of variations in speech sounds (and therefore learning ability) would clearly suffer from “altered organization of the representations of sound,” such as was found in the brains of rats that were lactationally-exposed to PCBs.

 

If the results of the animal experiment are relevant to effects on developing humans (which is a very strong possibility), a child’s learning ability would be expected to be related to the PCB exposure that occurs via human milk (see Figure 4); that kind of exposure has increased greatly (Figure 7) while learning disability increased by over 280,000 children, over the 14-year period during which breastfeeding and the accompanying transfers of PCBs were very rapidly increasing. (Figure 11)  And that exposure is by far greatest during the early months after birth, the specific period when the auditory function in the human brain is developing and therefore especially vulnerable.  This is in line with the increases that have been recorded.

 

Appendix E:  Estradiol, another neurodevelopmentally-important hormone, is also reduced by toxins that are present in human milk, and is reduced much more in males than in females:

Although estradiol is an estrogen, it is present in young boys at about two-thirds the level in girls, up to about age 11.109  According to the chair of the Department of Pharmocology at the University of Maryland, who also holds appointments in Physiology and Psychiatry and is author or coauthor of 234 publications, “Estradiol is a potent steroid… that exerts profound and enduring effects on the brain as it develops.”110  According to an extensive study on this general subject, “There are literally thousands of reports in the literature documenting that estradiol alters the expression of a multitude of genes in the brain.” 111

 

Given the above as well as the contents of Section 7, it should be apparent that both testosterone and estradiol are very important to the development of the brain.  It should therefore be of concern that both of these hormones are reduced in male infants by environmental toxins to which infants are very widely exposed; children are exposed to these toxins to a much greater or lesser extent depending on which type of infant feeding is chosen.  The chart below shows effects of developmental exposures of male rats to two of those toxins (PBDEs and PCBs), as found in a laboratory experiment.  The first and third charts show effects of the exposures on estradiol levels, and the second and fourth charts show effects on testosterone levels.  The white bars represent the comparison (unexposed) group of animals, and the other bars in each chart represent effects on groups exposed to PCBs and PBDEs, at higher and lower levels.

Fig. 12a

http://www.pollution-effects.info/index_files/image009.gif

 

As is apparent in the results shown in these charts, developmental exposures to both PBDEs and PCBs greatly reduced the levels of two different neurodevelopmentally-important hormones in male offspring.  This was the case despite the facts that the exposures were sufficiently low that they “did not affect reproductive success in dams or development of body weights in offspring at the doses tested,” and their effects on females were either insignificant or comparatively minor.

 

http://www.pollution-effects.info/index_files/image010.gifFig. 13

Seeing (above in Figure 12) the effects on levels of two neurologically-important hormones in male offspring that resulted from developmental exposure to PBDEs and PCBs, remember the dramatic differences in exposures to those toxins that are connected with type of infant feeding (see near beginnings of Sections 3.a and 3.b).  Figure 4 is repeated here for convenient reference regarding infant PCB exposure; remember that PCBs have been found to be present in human milk in doses 63 to 270 times the minimal risk level established by the U.S. Agency for Toxic Substances and Disease Registry.112

Also remember from Section 3.b (with references to sources),

  a) the evidence that PBDE levels in Americans have been at least as high as PCB levels, and

  b) data indicating that PBDEs have been found in infant formula in concentrations less than 3% as high as in average breast milk.

 

 

 Appendix F:  Additional links between pesticide exposures and autism:

In a 2014 study, proximity to agricultural fields with pesticide application during the developmental period was associated with greatly increased risk for ASD.138a  For organophosphates, odds ratios of autism increased without fail when going from first trimester through the second and third trimesters, for all of the exposure proximities studied (Table 3);  this was a distinct, strong upward trend, which could be anticipated to continue after birth in relation to exposures via lactation. (Unfortunately, data was not available for after birth.)  During the third trimester the odds of autism in relation to organophosphate pesticide exposures were doubled; exposures immediately following that third trimester, via breastfeeding, would very likely be in much more concentrated form than the prenatal transfers, 139e at a stage of recognized continued vulnerability to neurodevelopmental toxins (see Section 2).

 

Appendix G:  Other illustrations of the concentrating effect of  lactation:

Lead is one of the chemicals that (a) is normally present in human milk and (b) (in recent years) has been essentially absent in infant formula.(Section 3.e)  It doesn't accumulate in breast milk to multiples as high as is the case with the lipophilic toxins, but the increases in infant exposures via breastfeeding can nevertheless be substantial.  In a Chinese study, the mean concentration of lead in breast milk of twelve occupationally-lead-exposed women was found to be almost 12 times higher than that for the occupationally non-exposed population. (Li et al., Transfer of lead via placenta and breast milk in human, Biomed Environ Sci. 2000 Jun, http://www.ncbi.nlm.nih.gov/pubmed/11055009  In the only readily-found international comparison of lead levels in breast milk, the level in China was found to be two to 40 times as high as that in most other countries, with only Saudi Arabia being in near second place. (Winiarska-Mieczan, Cadmium, Lead, Copper and Zinc in Breast Milk in Poland, Biol Trace Elem Res. 2014; 157(1): 36–44. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3895183/  Table 6) 

  

Breastfeeding's property of magnifying concentrations of toxins can be especially disturbing if it is combined with major elevations in environmental exposures to the toxins, which obviously do occur.  For many years, Israeli dairy products contained 100 times the concentration of HCH (a pesticide) compared with similar products in the U.S.; the concentrations found in breast milk were estimated to be 800 times greater than those in U.S. dairy products. (Pohl and Tylenda, U.S. ATSDR, Breastfeeding exposure of infants to selected pesticides:  a public health viewpoint, Toxicology and Industrial Health (2000) 16, 65-77)  One way to look at the above is as follows:  International variation accounted for the first 100-fold difference, and breastfeeding accounted for 700 of the final 800-fold difference.

 

Compared with the increases quoted above, the following effect from combining breastfeeding with a typical exposure will seem fairly minor:  One study found that treatment of military homes with chlordane for pest control resulted in a fivefold increase of chlordane levels in the breast milk of nursing mothers.  (Pohl and Tylenda, U.S. ATSDR, Breastfeeding exposure of infants to selected pesticides: a public health viewpoint, Toxicology and Industrial Health (2000) 16, 65-77)  It should be kept in mind that the dose of pesticide to the infant from the breast milk would come in addition to the direct impact of the pesticide on the infant, who was likely to be breathing it in, possibly crawling on its residue, and engaging in hand-to-mouth activity.

 

 

 

References                         

1) The Surgeon General’s Call to Action to Support Breastfeeding 2011, p. 33, at www.surgeongeneral.gov/library/calls/breastfeeding/calltoactiontosupportbreastfeeding.pdf

2) The above Surgeon General's document, Table 2

 

3) See Section D of www.breastfeeding-benefits.net for details and many authoritative sources.

 

4) Houtrow et al., Changing Trends of Childhood Disability, 2001–2011, Pediatrics Vol. 134 No. 3 September 1, 2014 at http://pediatrics.aappublications.org/content/134/3/530.abstract

 

4b) Center on the Developing Child at Harvard University, National Scientific Council on the Developing Child:  Early Exposure to Toxic Substances Damages Brain Architecture, 2006, Working Paper No. 4; especially introduction, pp. 2, 7, 9;  link for this publication at http://developingchild.harvard.edu/resources/early-exposure-to-toxic-substances-damages-brain-architecture/  This Council is comprised of twelve leading scholars from all over the U.S.

 

5) Pastor et al., Diagnosed attention deficit hyperactivity disorder and learning disability:  United States 2004-2006, National Center for Health Statistics, 2008, at http://www.cdc.gov/nchs/data/series/sr_10/Sr10_237.pdf

 

6) Barouki et al., Developmental origins of non-communicable disease: Implications for research and public health, Environ Health. 2012; 11: 42. PMCID: PMC3384466  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3384466/

 

7) Di Renzo et al., International Federation of Gynecology and Obstetrics opinion on reproductive health impacts of exposure to toxic environmental chemicals, International Journal of Gynecology and Obstetrics, 2015, at http://www.figo.org/sites/default/files/uploads/News/Final%20PDF_8462.pdf

 

8)  NIH website on endocrine disruptors at www.niehs.nih.gov/health/topics/agents/endocrine

 

9)  Commission on Life Sciences, National Research Council:  Pesticides in the Diets of Infants and Children, p. 43, National Academy Press, Washington, D.C.  1993, at http://www.nap.edu/openbook.php?record_id=2126&page=43

 

9a)  See Section 1, cont. of www.disability-origins.info for details and citations of authoritative sources

 

10) Pages 98 and 125 in Improving the Risk Assessment of Persistent, Bioaccumulative, and Toxic Chemicals in Breast Milk, Workshop Summary Report, 2013, prepared for U.S. EPA by ICF International, at   http://cfpub.epa.gov/ncea/risk/recordisplay.cfm?deid=262210

 

11) Rice et al., Critical Periods of Vulnerability for the Developing Nervous System:  Evidence from Humans and Animal Models, EPA National Center for Environmental Assessment, at www.ncbi.nlm.nih.gov/pmc/articles/PMC1637807, p. 515

 

12) Pesticides in the Diets of Infants and Children,  p. 60, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C.  1993, at http://www.nap.edu/openbook.php?record_id=2126

 

13) WHO:  Principles for Evaluating Health Risks in Children Associated with Exposure to Chemicals, Environmental Health Criteria 237,  at http://www.inchem.org/documents/ehc/ehc/ehc237.pdf  Also see the expert statement in the introduction of the document in endnote 16a below about vulnerability when the brain is immature.

 

14) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1648530 and http://developingchild.harvard.edu/wp-content/uploads/2015/03/InBrief-The-Science-of-Early-Childhood-Development.pdf

 

 

15) WHO:  Principles for Evaluating Health Risks in Children Associated with Exposure to Chemicals, Environmental Health Criteria 237, See Figure 2, at http://www.inchem.org/documents/ehc/ehc/ehc237.pdf 

 

 

16)  According to the U.S. National Research Council, of the National Academies, 83% of the human brain’s growth spurt is postnatal. National Research Council (U.S.). Committee on Toxicology,  Recommendations for the Prevention of Lead Poisoning in Children, p. 19, at https://books.google.com/books? The following direct link might work:   id=15grAAAAYAAJ&printsec=frontcover&dq=Recommendations+for+the+Prevention+of+Lead+Poisoning+in+Children&hl=en&sa=X&ved=0CB4Q6AEwAGoVChMI06yW25q2xwIVjQqSCh2dsQ2G#v=onepage&q=Recommendations%20for%20the%20Prevention%20of%20Lead%20Poisoning%20in%20Children&f=false 

 

16a) Center on the Developing Child at Harvard University, National Scientific Council on the Developing Child:  Early Exposure to Toxic Substances Damages Brain Architecture, 2006, Working Paper No. 4; especially pp. 1 and 2;  link for this publication at http://developingchild.harvard.edu/resources/early-exposure-to-toxic-substances-damages-brain-architecture/  This Council is comprised of twelve leading scholars from all over the U.S.

 

16b) See Section 3 of www.disability-origins.info for details and citations of authoritative sources.

 

16c) See www.air-pollution-autism.info for details and authoritative sources.

 

16d) See Section 3.b above.

 

17) Jensen, A.A., Slorach, S.A.:  Chemical Contaminants in Human Milk, CRC Press, Inc., Boca Raton, Ann Arbor, Boston, 1991, p 15.  

For a more recent study finding disproportionate ratios between organohalogens in breast milk versus those in cord tissue and cord serum, see Needham et al., Partition of Environmental Chemicals between Maternal and Fetal Blood and Tissues, Environ Sci Technol. Feb 1, 2011; 45(3): 1121-1126,  at  http://pubs.acs.org/doi/pdf/10.1021/es1019614, Table 2, finding weight-based concentrations of organohalogens to be over 30 times higher in human milk than in umbilical cord tissue.

 

18) National Academies Press, Hormonally Active Agents in the Environment (1999), Chapter: 6:  Neurologic Effects, at http://www.nap.edu/read/6029/chapter/8#178, p. 178.  Describing studies measuring maternal concentrations of developmental toxins in 313 women in Michigan, this publication states, “The mean concentrations of PCBs were 6 ng/mL in maternal serum, 3 ng/mL in cord serum, and 841 ng/g in breast milk.”(p. 178)  From a German study (Winneke et al., 1998), “Mean concentrations of PCBs were 0.55 ng/mL in cord blood and 427 ng/g in the fat of breast milk.” (p. 183) (1 mL is about the same as 1 g when discussing a substance whose weight is about the same as that of water.)

 

18a) Kommission “Human-Biomonitoring” des Umweltbundesamtes:  Stoffmonographie PCB - Referenzwerte für Blut, Section 8.3.,found within https://www.umweltbundesamt.de/sites/default/files/medien/377/dokumente/pcbblut.pdf, website of Umwelt Bundes Amt (German Federal Environmental Office). The text drawn on says, " "Die derzeit durchschnittlich vom Erwachsenen täglich aufgenommene Menge an PCB (ca. 0,02 μg PCB/kg KG [13]) liegt deutlich unter der ATD von 1 μg PCB/kg KG. Der gestillte Säugling erhält dagegen eine deutlich höhere PCB-Zufuhr (3 μg PCB/kg KG.", which Bing Translator very respectably translates as " "The amount taken daily average currently by the adults of PCB (approx. 0.02 μg PCB/kg bw [13]) is well below the ATD of 1 μg PCB/kg. The breastfed infant, however, receives a significantly higher PCB intake (3 μg PCB/kg bw.)"

 

(18b) Birnbaum and Slezak, Dietary Exposure to PCBs and Dioxins in Children, Environmental Health Perspectives * Volume 107, Number 1, January 1999,  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566291/pdf/envhper00506-0029.pdf  

 

(18c) Exposure of young infants to environmental tobacco smoke: breast-feeding among smoking mothers.  Mascola,et al.,  Am J Public Health. 1998 June; 88(6): 893–896. PMCID: PMC1508233  found at www.ncbi.nlm.nih.gov/pmc/articles/PMC1508233

 

19) 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

 

20)  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 4.7.4.3,  at www.epa.gov/raf/publications/pdfs/PPKFINAL.PDF   According to these 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.

-- 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)  Stated that the half-life of methylmercury in the blood of lactating women is about half that in nonlactating women, apparently due to excretion in breast milk.

 -- Mercury Study Report to Congress c7o032-1-1,  EPA Office of Air Quality Planning & Standards and Office of Research and Development  Volume VII, Section 2.2.2.1,  at http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf   According to this EPA article, “Lactating women have shorter biological half-lives for methylmercury (average value 42 days), compared with nonlactating women (average value 79 days) (Greenwood et al., 1978). This is presumably a reflection of excretion of mercury into milk.

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

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

-- U.S. Hazardous Substances Data Bank of the National Library of Medicine's TOXNET system, at http://toxnet.nlm.nih.gov.    Evidence from the Iraqi poisoning incident showed that lactation decreased blood mercury clearance half-times in women by 44%, indicating rapid excretion of mercury in breast milk.

-- P. Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants,  Environmental Health Perspectives, accepted Oct. 1993   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1567218/pdf.  In this study by a prominent scientist (P. Grandjean) and his team, it was found that total mercury concentrations in infants that had been breastfed for one year were three times as high as those in infants that had not been breastfed.

-- Marques RC, et al., Hair mercury in breast-fed infants exposed to thimerosal-preserved vaccines. Eur J Pediatr. 2007 Sep;166(9):935-41. Epub 2007 Jan 20  This study found that mercury measured in infants’ hair increased 446% during the first six months of breastfeeding, while mercury measured  in the mothers’ hair decreased 57%. These measurements included mercury from vaccines (still containing mercury at that time in Brazil, where the study was carried out), which the authors estimated accounted for about 40% of the infants’ exposure during those six months.  Given that, combined with the finding in a Taiwanese study that over 95% of an infant’s exposure to mercury was from breastfeeding (Chien et al., 2006), the increase in the infants’ mercury levels attributable to breastfeeding was probably well over 200% during the first 6 months of breastfeeding. 

-- Rice et al., Environmental Mercury and Its Toxic Effects, J Prev Med Public Health. 2014 Mar; 47(2): 74–83, doi: PMCID: PMC3988285  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988285   According to these experts, the average whole body biological half-life of inhaled mercury is approximately 60 days, but it is estimated that the half-life of mercury in the brain can be as long as 20 years. The above findings of doubling and tripling of mercury levels in breastfed infants would have been based on levels in the whole body, where half-lives are relatively short and accumulation relatively minor, as opposed to levels in the especially vulnerable developing brain, where accumulation would be far greater.

 

21) Virgintino et al., Fetal Blood-Brain Barrier P-Glycoprotein Contributes to Brain Protection During Human Development, Journal of Neuropathology and Experimental Neurology, DOI: http://dx.doi.org/10.1097/nen.0b013e31815f65d9 50-61 First published online: 1 January 2008 at http://jnen.oxfordjournals.org/content/67/1/50.long

-- Young et al., Efflux transporters of the human placenta, Advanced Drug Delivery Reviews, Volume 55, Issue 1, 21 January 2003, Pages 125–132

 

21a)  Wang et al., Serum Concentrations of Selected Persistent Organic Pollutants in a Sample of Pregnant Females and Changes in Their Concentrations during Gestation, Environ Health Perspect. 2009 Aug; 117(8): 1244–1249, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721868/

 

22) P Grandjean and AA 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/ 

 

23) Oregon Department of Environmental Quality Environmental Cleanup Program, Oct. 2010, 10-LQ-023, p. D2-4 (attachment 2 of Appendix D, near very end) at http://www.deq.state.or.us/lq/pubs/docs/cu/HumanHealthRiskAssessmentGuidance.pdf 

Quoting, “The doses of PCBs that a breastfeeding infant may be expected to receive, given breast milk PCB concentrations measured in the literature, are presented in table 1. These doses range from 0.0019 to 0.0081 mg/kg/day and are 63-270 times higher than ATSDR’s minimal risk level (0.00003 mg/kg/day) for PCB exposures that last between 15 and 364 days.”

 

23a) Bell et al., Two-hit exposure to polychlorinated biphenyls at gestational and juvenile life stages:  Sex-specific neuromolecular effects in the brain, Molecular and Cellular Endocrinology, 20 (2016) 125, at http://www.sciencedirect.com/science/article/pii/S0303720715301489

 

24) Washington State Department of Ecology, Multiyear PBT Chemical Action Plan Schedule, 2007, at https://fortress.wa.gov/ecy/publications/documents/0707016.pdf, p. 64.

 

24a) Birnbaum and Slezak, Dietary Exposure to PCBs and Dioxins in Children, Environmental Health Perspectives * Volume 107, Number 1, January 1999,  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566291/pdf/envhper00506-0029.pdf

 

25) 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

 

25a) Environ Health Perspect. 2012 Jul; 120(7): 944–951, Published online 2012 Apr 25. doi:  10.1289/ehp.1104553, Review:  Tipping the Balance of Autism Risk: Potential Mechanisms Linking Pesticides and Autism, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404662/

 

26) Stewart et al., The Relationship between Prenatal PCB Exposure and Intelligence (IQ) in 9-Year-Old Children, Environ Health Perspect. 2008 Oct; 116(10): 1416–1422,  PMCID: PMC2569105 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2569105

 

27)  EPA:   Biomonitoring, Polychlorinated biphenyls (PCBs), at https://www.epa.gov/sites/production/files/2015-05/documents/biomonitoring-pcbs.pdf    For other details and sources, see Section 1.b.f of www.breastfeeding-vs-formula.info

 

27a)  Verner et al., Measured Prenatal and Estimated Postnatal Levels of Polychlorinated, Biphenyls (PCBs) and ADHD-Related Behaviors in 8-Year-Old Children, Environ Health Perspec, Sept. 2015, at http://ehp.niehs.nih.gov/1408084/

 

28) Verner et al., Measured Prenatal and Estimated Postnatal Levels of Polychlorinated Biphenyls (PCBs) and ADHD-Related Behaviors in 8-Year-Old Children, Figure 2, Environ Health Perspect; DOI:10.1289/ehp.1408084 , Vol. 123, Issue 9, Sept. 2015, at http://ehp.niehs.nih.gov/1408084

 

29)  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

--Jacobson et al., Determinants of polychlorinated biphenyls (PCBs), polybrominated biphenyls (PBBs), and dichlorodiphenyl trichloroethane (DDT) levels in the sera of young children, Am J Public Health. 1989 October; 79(10): 1401–1404

-- Table 1 in Jusko et al., Prenatal and Postnatal Serum PCB Concentrations and Cochlear Function in Children at 45 Months of Age, Environmental Health Perspectives, 22 July 2014 (Advance Pub.) at http://ehp.niehs.nih.gov/wp-content/uploads/advpub/2014/7/ehp.1307473.pdf 

-- Danish Health and Medicines Authority, Health risks of PCB in the indoor climate in Denmark, 2013, at http://sundhedsstyrelsen.dk/~/media/D290AF38C2114775804F1B6BDD6841C6.ashx

-- Ayotte et al., Assessment of Pre- and Postnatal Exposure to Polychlorinated Biphenyls:

Lessons from the Inuit Cohort Study, Environmental Health Perspectives • Volume 111 | Number 9 | July 2003, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241583/pdf/ehp0111-001253.pdf (finding 6.6-fold increase in infant PCB levels with over three months of breastfeeding, compared with no breastfeeding -- see Table 4)

-- Trnovec et al., Assessment of exposure to PCB 153 from breast feeding and normal food intake in individual children using a system approach model, Chemosphere, Dec. 2011, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228605/

 

30) Rogan et al., Polychlorinated Biphenyls (PCBs) and Dichlorodiphenyl Dichloroethene (DDE) in Human Milk:  Effects of Maternal Factors and Previous Lactation, American Journal of Public Health, A1JPH February 1986, Vol. 76, No. 2, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1646471/pdf/amjph00265-0062.pdf

 

30a)  Jusko et al.,  Prenatal and Postnatal Serum PCB Concentrations and Cochlear Function in Children at 45 Months of Age, Environmental Health Perspectives, 22 July 2014 (Advance Pub.) at http://ehp.niehs.nih.gov/wp-content/uploads/advpub/2014/7/ehp.1307473.pdf

 

30b) U.S. ATSDR  Public Health Statement for Polychlorinated Biphenyls (PCBs),  November 2000,  at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf,  p. 569

 

31) Kenet et al., Perinatal exposure to a noncoplanar polychlorinated biphenyl alters tonotopy, receptive fields, and plasticity in rat primary auditory cortex, 2007, The National Academy of Sciences of the USA, 7646–7651, PNAS, May 1, 2007, vol. 104, no. 18, at http://www.pnas.org/content/104/18/7646.full.pdf at http://www.pnas.org/content/104/18/7646.full.pdf

 

Re Dr. Merzenich:  see http://www.brainhq.com/world-class-science/science-team/dr-michael-merzenich

 

32) Merzenich, What underlies the documented increase in autism incidence? Results of a new study,  from On the Brain, by Dr. Michael Merzenich, 26 April 2007, at http://www.onthebrain.com/2007/04/underlies-documented-increase-autism-incidence-results-new-study

 

32a) Science News/Autism Speaks, 20 April 2016, Meeting highlights from the Interagency Autism Coordinating Committee; summary of presentation by Dr. Paul Lipkin and Kiely Law of Interactive Autism Network, of preliminary findings of a study; www.autismspeaks.com

 

33) at  http://developingchild.harvard.edu/about/who-we-are/history-of-the-center

 

34) National Scientific Council on the Developing Child, Science Briefs: Prenatal and Infant Exposure to an Environmental Pollutant Damages Brain Architecture and Plasticity (2007). at  http://www.policyarchive.org/handle/10207/20626

 

35) University of California at San Francisco:  Breastfeeding, Brain Development and Chemical Poisons: Neuroscientist Michael Merzenich, By Jeff Miller, May 18, 2007  at https://www.ucsf.edu/news/2007/05/3817/merzenich

 

36) WHO, Persistent Organic Pollutants:  Impact on Child Health, p. 6, at http://whqlibdoc.who.int/publications/2010/9789241501101_eng.pdf

 

37) Class of PCBs causes developmental abnormalities in rat pups, UCSF News Center, Univ. of California San Francisco, by Jennifer O’Brien, April 23, 2007, at  http://www.ucsf.edu/news/2007/04/5564/class-pcbs-causes-developmental-abnormalities-rat-pupsat

 

37a)  CDC web page, Breastfeeding:  Exposure to Environmental Toxins, at http://www.cdc.gov/breastfeeding/disease/environmental_toxins.htm

 

37b) AAP Policy Statement, Pediatrics, Mar. 2012, Vol. 129, Issue 3, Breastfeeding and the Use of Human Milk, at http://pediatrics.aappublications.org/content/129/3/e827.full#content-block

 

37c) Bennetto et al., Children with autism spectrum disorder have reduced otoacoustic emissions at the 1 kHz mid-frequency region, Autism Research, at http://onlinelibrary.wiley.com/doi/10.1002/aur.1663/abstract.  Also an article in Medline Plus, Aug. 1, 2016, R. Preidt,"Hearing Test May Predict Autism Risk Sooner:  Study" at https://medlineplus.gov/news/fullstory_160181.html

 

37d) Jusko et al., Prenatal and Postnatal Serum PCB Concentrations and Cochlear Function in Children at 45 Months of Age, Environ Health Perspect, 2014, at http://ehp.niehs.nih.gov/wp-content/uploads/advpub/2014/7/ehp.1307473.pdf

 

38) Table 2 of Boucher et al., Prenatal Exposure to Polychlorinated Biphenyls: A Neuropsychologic Analysis, Environ Health Perspect v.117(1); 2009 Jan at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627868

 

38a) Boucher et al., Prenatal Exposure to Polychlorinated Biphenyls: A Neuropsychologic Analysis, Environ Health Perspect v.117(1); 2009 Jan at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627868

 

38b) Coccini et al., Perinatal co-exposure to methylmercury and PCB153 or PCB126 in rats alters the cerebral cholinergic muscarinic receptors at weaning and puberty, Toxicology, 2007 Aug 16;238(1):34-48. Epub 2007 May 25, at https://www.ncbi.nlm.nih.gov/pubmed/17618726

 

38c) For translating Rat PND 10 and PND 36 to human equivalent ages:  Workman AD, Charvet CJ, Clancy B, Darlington RB, Finlay BL. 2013. Modeling transformations of neurodevelopmental sequences across mammalian species. J Neurosci. 33: 7368-7383, at  http://www.translatingtime.net/  

 

38d) ATSDR web page on DDT at http://www.atsdr.cdc.gov/PHS/PHS.asp?id=79&tid=20

 

38e) Rice et al., Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models, p. 525  at  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1637807/pdf/envhper00312-0143.pdf

 

38f) Bernard Weiss, 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  

Very much the same message is presented in Giordano et al., Review Article, Developmental Neurotoxicity: Some Old and New Issues, International Scholarly Research Network, ISRN Toxicology Volume 2012, Article ID 814795, doi:10.5402/2012/814795 at http://www.hindawi.com/isrn/toxicology/2012/814795/ref/

 

38g) WHO, Children's health and the environment, A global perspective, at http://apps.who.int/iris/bitstream/10665/43162/1/9241562927_eng.pdf

 

38h) U.S. Agency for Toxic Substances & Disease Registry:  Lead Toxicity, accessed July 2016, at http://www.atsdr.cdc.gov/csem/csem.asp?csem=7&po=10

 

38k) Wiggins et al., Autism Spectrum Disorder Symptoms Among Children Enrolled in the Study  to Explore Early Development (SEED), J Autism Dev Disord. 2015 Oct; 45(10): 3183–3194.

 

38m) Eriksson et al., Polybrominated Diphenyl Ethers, A Group of Brominated Flame

Retardants, Can Interact with Polychlorinated Biphenyls in Enhancing

Developmental Neurobehavioral Defects, TOXICOLOGICAL SCIENCES 94(2), 302–309 (2006) doi:10.1093/toxsci/kfl109, Advance Access publication September 15, 2006, at http://toxsci.oxfordjournals.org/content/94/2/302.full.pdf+html

 

38n) Pesticides in the Diets of Infants and Children, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C.  1993, p. 7

 

39) Danish Health and Medicines Authority, Health risks of PCB in the indoor climate in Denmark, 2013, at http://sundhedsstyrelsen.dk/~/media/D290AF38C2114775804F1B6BDD6841C6.ashx

40) EPA:  Flame Retardant Alternatives for Hexabromocyclododecane (HBCD) , Final Report, June 2014, EPA Publication 740R14001, p. iv, at http://www.epa.gov/sites/production/files/2014-06/documents/hbcd_report.pdf

 

41) Abdallah et al., Tetrabromobisphenol-A, hexabromocyclododecane and its degradation products in UK human milk: Relationship to external dose. Environment International, 2010, including Table 2 for 95th percentile figure, at http://dx.doi.org/10.1016/j.envint.2010.11.008

 

42) ATSDR: Public Health Statement for PBDEs, CAS#: 67774-32-7, (summary chapter from the Toxicological Profile for PBDEs) at http://www.atsdr.cdc.gov/phs/phs.asp?id=1449&tid=183

 

43) 2009 EPA Polybrominated Diphenyl Ethers Action Plan at  http://www.epa.gov/sites/production/files/2015-09/documents/pbdes_ap_2009_1230_final.pdf, p. 12

 

43b)  Herbstman et al., Developmental Exposure to Polybrominated Diphenyl Ethers and Neurodevelopment. Curr Environ Health Rep. 2014 Jun 1;1(2):101-112.  at http://www.ncbi.nlm.nih.gov/pubmed/25530937

 

43c)  Bellanger et al., Neurobehavioral Deficits, Diseases, and Associated Costs of Exposure to Endocrine-Disrupting Chemicals in the European Union, J Clin Endocrinol Metab. 2015 Apr; 100(4): 1256–1266, Published online 2015 Mar 5. doi:  10.1210/jc.2014-4323  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4399309/

 

44) Wang et al., Emission estimation and congener-specific characterization of polybrominated diphenyl ethers from various stationary and mobile sources, Environmental Pollution, Vol. 158, issue 10, Oct. 2010, pp. 3108-3115 at http://www.sciencedirect.com/science/article/pii/S0269749110002769 ; also  Wang et al., Polybrominated diphenyl ethers in various atmospheric environments of Taiwan: Their levels, source identification and influence ofcombustion sources, Chemosphere, Volume 84, Issue 7, Aug. 2011  at http://www.sciencedirect.com/science/article/pii/S0045653511006515

 

45) 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

 

46)  Also Wang et al., Emission estimation and congener-specific characterization of polybominated diphenyl ethers from various stationary and mobile sources, Environmental Pollution, Vol. 168, Oct. 2010

 

47) at http://www.fhwa.dot.gov/planning/census_issues/archives/metropolitan_planning/cps2k.cfm

 

48)  Law et al., Levels and trends of HBCD and BDEs in the European and Asian environments, with some information for other BFRs, chemosphere.2008.02.066. Epub 2008 May 9.at http://www.ncbi.nlm.nih.gov/pubmed/18472134

  

50)  EPA: Assessing and Managing Chemicals under TSCA: Polybrominated Diphenyl Ethers (PBDEs)

at http://www.epa.gov/assessing-and-managing-chemicals-under-tsca/polybrominated-diphenyl-ethers-pbdes

 

51)   2009 EPA Polybrominated Diphenyl Ethers Action Plan at  http://www.epa.gov/sites/production/files/2015-09/documents/pbdes_ap_2009_1230_final.pdf, p. 12

  

54) Carrizo et al. 2007. Influence of breastfeeding in the accumulation of polybromodiphenyl ethers during the first years of child growth. Environ Sci Technol 41(14):4907-4912.)

 

55) Re PBDEs in breast milk:  mean of 1916 pg/g wwt, in Table 5 of  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  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

 

56) “Food and beverages” row in Table 1 of Health Canada:  Human Health State of the Science Report on Decabromodiphenyl Ether (decaBDE), Dec. 2012,  at https://www.ec.gc.ca/ese-ees/92D49BA9-4B11-4C56-BDB0-9A725C5F688E/DecaBDE%20-%20Final%20SoS%20-%20EN.pdf

 

56a)  Roze et al., Prenatal Exposure to Organohalogens, Including Brominated Flame Retardants, Influences Motor, Cognitive, and Behavioral Performance at School Age, Environmental Health Perspect, Dec. 2009

 

57) 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

 

58) Gascon et al., Polybrominated Diphenyl Ethers (PBDEs) in Breast Milk and Neuropsychological Development in Infants   US National Library of Medicine National Institutes of Health  Environ Health Perspect  v.120(12); Dec 2012 > PMC3548276   Environ Health Perspect. 2012 December; 120(12): 1760–1765.  at www.ncbi.nlm.nih.gov/pmc/articles/PMC3548276

 

58a) In the first study described, the comparisons were made between children with detectable levels of PBDEs versus those without detectable levels; in the second one, the basic comparisons were made among three different groups according to levels of exposure, with the most-exposed group being made up of over 40% of the population; comparisons were made between those in which the PBDE level was quantifiable, those in which it was undetectable, and those in which it was detectable but not quantifiable.(Table 2 of Gascon et al. 2012)

 

59) Chao et al., Levels of Breast Milk PBDEs From Southern Taiwan and Their Potential Impact on Neurodevelopment, Pediatric Research (2011) 70, 596–600; doi:10.1203/PDR.0b013e3182320b9b  at  http://www.nature.com/pr/journal/v70/n6/pdf/pr20111086a.pdf?origin=publication_detail

 

60) 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. 2006 Oct; 114(10): 1515–1520.Published online 2006 Jul 13. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1626425

 

61) Gong et al., Potential risk assessment of polybrominated diphenyl ethers (PBDEs) by consuming animal-derived foods collected from interior areas of China, Environ Sci Pollut Res Int, 2015 Jun;22(11):8349-58. at http://www.ncbi.nlm.nih.gov/pubmed/25537283 

 

63) Carignan et al., Predictors of Tetrabromobisphenol-A (TBBP-A) and Hexabromocyclododecanes (HBCD) in Milk from Boston Mothers, Environ Sci Technol. 2012 Nov 6; 46(21): 12146–12153.PMCID: PMC3500145 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3500145

 64) Carignan study just above, especially Table 2

 

65)  Antignac et al., Exposure assessment of fetus and newborn to brominated flame retardants in France: preliminary data, Mol Nutr Food Res., 2008 Feb;52(2):258-65. doi: 10.1002/mnfr.200700077, abstract at http://www.ncbi.nlm.nih.gov/pubmed/18186099

 

66) Croes et al., Persistent organic pollutants (POPs) in human milk: A biomonitoring study in rural areas of Flanders (Belgium), Chemosphere 89 (2012) 988–994, at http://www.ncbi.nlm.nih.gov/pubmed/22840535

 

67) Stapleton et al., Alternate and New Brominated Flame Retardants Detected in U.S. House Dust, Environ. Sci. Technol., 2008, 42 (18), pp 6910–6916, at http://pubs.acs.org/doi/abs/10.1021/es801070p

 

68) Abdallah et al., Hexabromocyclododecanes and Tetrabromobisphenol-A in Indoor Air and Dust in Birmingham, UK: Implications for Human Exposure, Environ. Sci. Technol., 2008, 42 (18), pp 6855–686, DOI: 10.1021/es801110a, at http://pubs.acs.org/doi/abs/10.1021/es801110a

 

69) Lorber M. Exposure of Americans to polybrominated diphenyl ethers. J Expo Sci Environ Epidemiol. 2008;18(1):2–19. [PubMed] at http://www.ncbi.nlm.nih.gov/pubmed/17426733; 

 

70) Johnson et al., Associations between brominated flame retardants in house dust and hormone levels in men, Sci Total Environ. 2013 Feb 15; PMCID: PMC3572297, 445-446: 177–184.at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3572297/     

-- Ni et al., A review of human exposure to polybrominated diphenyl ethers (PBDEs) in China, Int. J Hyg Environ Health,  2013, Nov.,  216(6):607-23,  doi: 10.1016/j.ijheh.2013.02.002. Epub 2013 Mar 13, at http://www.ncbi.nlm.nih.gov/pubmed/23491027

 

71) Roosens et al., Exposure to Hexabromocyclododecanes (HBCDs) via Dust Ingestion, but Not Diet, Correlates with Concentrations in Human Serum: Preliminary Results,, Environ Health Perspect; DOI:10.1289/ehp.0900869 -- this study with Belgian adults found that HBCD levels were correlated with household dust

 

72) Re persistence, see http://ehp.niehs.nih.gov/1204993; HBCD as organohalogen is common knowledge.

 

73) Environment Canada, Health Canada, Appendix E of Appendix of the Screening Assessment Report on

Hexabromocyclododecane, Chemical Abstracts Service Registry Number 3194-55-6, November 2011

at http://www.ec.gc.ca/ese-ees/default.asp?lang=En&n=03991FB3-1

 

73a) Re: EPA’s RfD for dioxin:  In EPA’s Reanalysis of Key Issues Related to Dioxin Toxicity and Response to NAS Comments, Volume 1, EPA/600/R-10/038F www.epa.gov/iris at http://cfpub.epa.gov/ncea/iris/iris_documents/documents/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)  

 

Re: breastfed infants’ exposures to dioxins, in many nations:

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

U.K. Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment:  COT Statement on a toxicological evaluation of chemical analyses carried out as part of a pilot study for a breast milk archive, 2004, Table 1 and item 41, at http://cot.food.gov.uk/pdfs/cotsuremilk.pdf

 

- Lorber et al., Infant Exposure to Dioxin-like Compounds in Breast Milk, Vol. 110 No. 6, June 2002,  Environmental Health Perspectives at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download, indicating 242 pg of TEQ/kg-d at initiation of breastfeeding.

 

-  Costopoulou, Infant dietary exposure to dioxins and dioxin-like compounds in Greece, Food and Chemical Toxicology  Volume 59, September 2013, Pages 316–324, at http://www.sciencedirect.com/science/article/pii/S0278691513003803

 

 - 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

- 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

 - 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

 

74) 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

For the EPA’s RfD for dioxins, to compare the doses indicated in this article to RfD, see 73a above.

 

75) 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://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240886/pdf/ehp0110-a00325.pdf,  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

 

76) Mocarelli et al., Perinatal Exposure to Low Doses of Dioxin Can Permanently Impair Human Semen Quality, Environ Health Perspect. May 2011; 119(5): 713–718. Published online Jan 24, 2011. doi:  10.1289/ehp.1002134  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3094426/

 

77) In the Results section, “Serum TCDD concentrations measured at the time of this study in the exposed breast- and formula-fed groups (average, 2.4 ppt and 1.1 ppt, respectively) and their respective comparison groups (average, 1.8 ppt and 1.0 ppt, respectively)

 

79) Abraham et al., POP accumulation in infants during breast-feeding. Organohalogen Compounds 48:25–26 (2000), as reported in Infant Exposure to Dioxin-like Compounds in Breast Milk  Lorber et al., Vol.110 | No. 6 | June 2002 • Environmental Health Perspectives at  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240886/pdf/ehp0110-a00325.pdf

 

80) 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, Tables 2 and 3, at http://jech.bmj.com/content/61/7/591.full.pdf+html.  See the “Adjusted OR” line, with “Referent” (meaning 1) for the groups with non-detectable dioxins, versus the Adjusted OR’s for the groups with detectable dioxins. (In each chart, the second and third chemicals listed are dioxins).

 

80a) Polanska et al., Review of current evidence on the impact of pesticides, polychlorinated biphenyls and selected metals on attention deficit /hyperactivity disorder in children, Int J Occup Med Environ Health. <#> 2013 Mar;26(1):16-38. doi:10.2478/s13382-013-0073-7. Epub 2013 Mar 22, at http://www.ncbi.nlm.nih.gov/pubmed/23526196  

 

81) Mercury typically 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)

 

82) 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

 

83) 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 http://academic.research.microsoft.com/Publication/57536306/survey-of-total-mercury-in-infant-formulae-and-oral-electrolytes-sold-in-canada

 

83a) Gilbert et al., Neurobehavioral effects of developmental methylmercury exposure, Environ Health Perspect. 1995 Sep;103 Suppl 6:135-42, at http://www.ncbi.nlm.nih.gov/pubmed/8549462

 

84) 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

 

85)  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 4.7.4.3,  at www.epa.gov/raf/publications/pdfs/PPKFINAL.PDF   According to these 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.

-- 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)  Stated that the half-life of methylmercury in the blood of lactating women is about half that in nonlactating women, apparently due to excretion in breast milk.

 -- Mercury Study Report to Congress c7o032-1-1,  EPA Office of Air Quality Planning & Standards and Office of Research and Development  Volume VII, Section 2.2.2.1,  at http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf   According to this EPA article, “Lactating women have shorter biological half-lives for methylmercury (average value 42 days), compared with nonlactating women (average value 79 days) (Greenwood et al., 1978). This is presumably a reflection of excretion of mercury into milk.

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

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

-- U.S. Hazardous Substances Data Bank of the National Library of Medicine's TOXNET system, at http://toxnet.nlm.nih.gov.    Evidence from the Iraqi poisoning incident showed that lactation decreased blood mercury clearance half-times in women by 44%, indicating rapid excretion of mercury in breast milk.

-- P. Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants,  Environmental Health Perspectives, accepted Oct. 1993   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1567218/pdf.  In this study by a prominent scientist (P. Grandjean) and his team, it was found that total mercury concentrations in infants that had been breastfed for one year were three times as high as those in infants that had not been breastfed.

-- Marques RC, et al., Hair mercury in breast-fed infants exposed to thimerosal-preserved vaccines. Eur J Pediatr. 2007 Sep;166(9):935-41. Epub 2007 Jan 20  This study found that mercury measured in infants’ hair increased 446% during the first six months of breastfeeding, while mercury measured  in the mothers’ hair decreased 57%. These measurements included mercury from vaccines (still containing mercury at that time in Brazil, where the study was carried out), which the authors estimated accounted for about 40% of the infants’ exposure during those six months.  Given that, combined with the finding in a Taiwanese study that over 95% of an infant’s exposure to mercury was from breastfeeding (Chien et al., 2006), the increase in the infants’ mercury levels attributable to breastfeeding was probably well over 200% during the first 6 months of breastfeeding. 

 

85a) 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, Volume 84, Issue 2, October 2000, Pages 186–194, Table 1

 

85b) Eriksson et al., Polybrominated Diphenyl Ethers, A Group of Brominated Flame Retardants, Can Interact with Polychlorinated Biphenyls in Enhancing Developmental Neurobehavioral Defects, Toxicological Sciences 94(2), 302–309 (2006) doi:10.1093/toxsci/kfl109, Advance Access publication September 15, 2006, in second from final paragraph, at http://toxsci.oxfordjournals.org/content/94/2/302.full.pdf+html

 

85c) Al-Saleh et al., Predictors of mercury (HG) exposure in breast-fed infants, Conference on Environment and Health Basel 2013, at http://www.iseepi.org/Conferences/Docs/2013_Basel_Abstracts.pdf

 

85d) Verner et al., Measured Prenatal and Estimated Postnatal Levels of Polychlorinated, Biphenyls (PCBs) and ADHD-Related Behaviors in 8-Year-Old Children, Environ Health Perspec, Sept. 2015, at http://ehp.niehs.nih.gov/1408084/

 

86) McCann, Mercury Levels in Blood from Newborns in the Lake Superior Basin, GLNPO ID 2007-942 November 30, 2011, at http://www.health.state.mn.us/divs/eh/hazardous/topics/studies/glnpo.pdf  According to the author, “the percentage of participants with mercury levels above the RfD in this study (in the U.S. Midwest) is similar to that for women of childbearing age who participated in (U.S.) National Health and Nutrition Examination Survey (NHANES) (Mahaffey et al., 2009).”

 

87) Mahaffey et al., Blood organic mercury and dietary mercury intake: National Health and Nutrition Examination Survey, 1999 and 2000, Environ Health Perspect.  2004 Apr;112(5):562-70.at http://www.ncbi.nlm.nih.gov/pubmed/15064162

 

88) Center on the Developing Child, Harvard Univ.:  The Science of Early Childhood Development, at http://developingchild.harvard.edu/wp-content/uploads/2015/05/Science_Early_Childhood_Development.pdf 

 

89) Adams et al., Toxicological status of children with autism vs. neurotypical children and the association with autism severity, Biol Trace Elem Res., 2013 Feb;151(2):171-80. doi: 10.1007/s12011-012-9551-1. Epub 2012 Nov 29. abstract at http://www.ncbi.nlm.nih.gov/pubmed/23192845 , full text at http://www.rescuepost.com/files/adams-et-al-2012-tox-status-of-asd-children-blood-and-urine.pdf

 

90) Mercury Study Report to Congress c7o032-1-1,  Office of Air Quality Planning & Standards and Office of Research and Development  Volume VII, Section 2.2.2.1,  at http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf

 

90a) WHO, Environment and Health Information System (ENHIS), 4.4, Exposure to chemical hazards in Food, at http://data.euro.who.int/eceh-enhis/Default2.aspx?indicator_id=18

 

91) U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury,  at http://www.atsdr.cdc.gov/toxprofiles/tp46.pdf, Section 2.2.2.6, p. 146 

 

92) Mahaffey et al., Blood Organic Mercury and Dietary Mercury Intake: National Health and Nutrition Examination Survey, 1999 and 2000, Environmental Health Perspectives, volume 112 | number 5 | April 2004, top lines of Tables 2 and 4, 75th, 90th and 95th percentile columns, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241922/pdf/ehp0112-000562.pdf ; the authors point out that organic mercury in human blood is predominantly methylmercury.

-- Also, according to 2003 data from the U.S. National Center for Health Statistics, among the many women who have total blood mercury levels exceeding the safe level established by the EPA (5.8 mcg/L), over 90% of the total mercury was found to be “organic/methyl mercury.” See Figure 1 of Mahaffey et al. study just cited.

-- Also see http://toxics.usgs.gov/definitions/methylmercury.html

 

93) EPA-452/R-97-009 December 1997  p. 5-29 (Section 5.6.1) at http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf

 

93a) U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury  at www.atsdr.cdc.gov/toxprofiles/tp46.pdf,  p. 17

 

93b) U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury  at http://www.atsdr.cdc.gov/toxprofiles/tp46.pdf, Section 1.6 

 

93c) D.C. Bellinger et al., Environmental Pollutant Exposures and Children's Cognitive Abilities,  in Environmental Effects on Cognitive Abilities, Robert J Sternberg, PhD, ed., Psychology Press,  pp. 159, 162 t  https://books.google.com/books?hl=en&lr=&id=9tZ4AgAAQBAJ&oi=fnd&pg=PA157&dq=greater+concentration+of+heavy+metals+lead+and+mercury+in+human+breast+milk&ots=mUIx6jLceV&sig=zBcjI4ZorcYiYjNjKa5vP-wJizQ#v=onepage&q&f=false

 

94) 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

Also Priya et al., 2011, 1999a. Toxicological Profile for Mercury Level of trace elements (copper, zinc, magnesium and selenium) and toxic elements (lead and mercury) in the hair and nail of children with autism. Biol Trace Elem Res. 2011;142:148–158;  

Also Hassanien et al., Environmental Heavy Metals and Mental Disorders of Children in Developing Countries. Environm Risk. 2011;1:1–25.;.

Also El-Baz et al., Hair Mercury Measurement in Egyptian Autistic Children. Egypt J Med Human Gen. 2010;11:135–141;

Also Al-Farsi et al., Levels of heavy metals and essential minerals in hair samples of children with autism in Oman: a case-control study (2013)

 

95) Adams et al., Mercury, lead, and zinc in baby teeth of children with autism versus controls, J Toxicol Environ Health A., 2007 Jun;70(12):1046-51.at http://www.ncbi.nlm.nih.gov/pubmed/17497416

 

96) Chien LC, et al., Analysis of the health risk of exposure to breast milk mercury in infants in Taiwan. Chemosphere. 2006 Jun;64(1):79-85. Epub 2006 Jan 25 at http://www.ncbi.nlm.nih.gov/pubmed/16442149

 

97) Windham et al., Autism Spectrum Disorders in Relation to Distribution of Hazardous Air Pollutants in the San Francisco Bay Area, Environ Health Perspect. 2006 Sep; 114(9): 1438–1444. Published online 2006 Jun 21. doi:  10.1289/ehp.9120 PMCID: PMC1570060 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1570060/

 

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

 

98a) EPA web page on Lead and lead compounds (inorganic), accessed June, 2016, at https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=277

 

98b) U.S. FDA:  Total Diet Study -- Market Baskets 2006-2011, p. 68, items 202 and 203, at http://www.fda.gov/downloads/Food/FoodScienceResearch/TotalDietStudy/UCM184301.pdf

  Also FDA publication, Lead and Pregnancy, at http://www.cdc.gov/nceh/lead/publications/leadandpregnancy2010.pdf, p. 102.

 

98c) U.S. Food and Drug Administration:  Lipstick & Lead: Questions & Answers,  at http://www.fda.gov/Cosmetics/ProductsIngredients/Products/ucm137224.htm#q2

98d)  As reported in Ettinger et al., Effect of breast milk lead on infant blood lead levels at 1 month of age, Environ Health Perspect. 2004 Oct; at http://www.ncbi.nlm.nih.gov/pubmed/15471729

 

98d1)  Gulson et al.,  Longitudinal study of daily intake and excretion of lead in newly born infants, Environ Res., 2001 Mar;85(3):232-45. at http://www.ncbi.nlm.nih.gov/pubmed/11237512  Table 4. 

 

98d2)  Gulson et al., Relationships of Lead in Breast Milk to Lead in Blood, Urine, and Diet of the

Infant and Mother, Environmental Health Perspectives * Volume 106, Number 10, October 1998, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1533188/pdf/envhper00533-0085.pdf

 

98d3) Ettinger et al., Maternal Blood, Plasma, and Breast Milk Lead: Lactational Transfer and Contribution to Infant Exposure, Environ Health Perspect, 2014, DOI:10.1289/ehp.1307187 at http://ehp.niehs.nih.gov/1307187/

 

98e)  CDC web page on lead at http://www.cdc.gov/nceh/lead/

 

98e1) Burns and Gerstenberger, Implications of the New Centers for Disease Control and Prevention Blood Lead Reference Value, Am J Public Health, v.104(6); Jun 2014 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4062025/

 

98f) Li et al., Transfer of lead via placenta and breast milk in human, Biomed Environ Sci,, 2000 Jun;13(2):85-9, at http://www.ncbi.nlm.nih.gov/pubmed/11055009

 

98g)  American Academy of Pediatrics Policy Statement:  Prevention of Childhood Lead Toxicity, June  2016, at http://pediatrics.aappublications.org/content/early/2016/06/16/peds.2016-1493

 

98f1) CDC data at https://www.cdc.gov/breastfeeding/pdf/2014breastfeedingreportcard.pdf

 

98g1) Table 9-3 of CDC:  Guidelines for the identification and management of lead exposure in pregnant and lactating women, at http://www.cdc.gov/nceh/lead/publications/leadandpregnancy2010.pdf

 

98g2) Gulson et al., Relationships of Lead in Breast Milk to Lead in Blood, Urine, and Diet of the Infant and Mother, Environmental Health Perspectives * Volume 106, Number 10, October 1998, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1533188/pdf/envhper00533-0085.pdf

 

 

98g6) Tau et al., Normal Development of Brain Circuits, Neuropsychopharmacology, v.35(1); 2010 Jan at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055433/, indicating hand-to-mouth activity beginning at 6 months.

 

98g3)  p. 109 of CDC:  GUIDELINES FOR THE IDENTIFICATION AND MANAGEMENT OF LEAD EXPOSURE IN PREGNANT AND LACTATING WOMEN, at http://www.cdc.gov/nceh/lead/publications/leadandpregnancy2010.pdf

 

98g4) Canfield et al., Intellectual Impairment in Children with Blood Lead Concentrations below 10 μg per Deciliter, New England Journal of Med., 2003, Figure 1.

 

98g5)  Ris et al., Early exposure to lead and neuropsychological outcome in adolescence. J Int Neuropsychol Soc. 2004;10:261–70.

 

98h) According to the U.S. ATSDR, "Organic lead (tetramethyllead) is more likely to be absorbed through the skin than inorganic lead."  ATSDR web page at http://www.atsdr.cdc.gov/csem/csem.asp?csem=7&po=6

 

98h1) Sakamoto et al.,Changes in body burden of mercury, lead, arsenic, cadmium and selenium in infants during early lactation in comparison with placental transfer,

Ecotoxicol Environ Saf. 2012 Oct;84:179-84. doi: 10.1016/j.ecoenv.2012.07.014. Epub 2012 Jul 30.

 

98h2) Chen et al., Placental transfer and concentrations of cadmium, mercury, lead, and selenium in mothers, newborns, and young children, J Expo Sci Environ Epidemiol. 2014 Sep-Oct; 24(5): 537–544. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4329243/

 

98i) Cinar et al., In which regions is breast-feeding safer from the impact of toxic elements from the environment? Bosn J Basic Med Sci. 2011 Nov; 11(4): 234–239. PMCID: PMC4362578

 

98j) U.S. FDA web page at

www.fda.gov/Cosmetics/ProductsIngredients/PotentialContaminants/ucm388820.htm

 

98k) Gulson et al., Dietary Lead Intakes for Mother/Child Pairs and Relevance to

Pharmacokinetic Models, Env. Health Perspect, Vol. 105, No. 12, Dec. 1997

 

98m) Manton et al., Release of lead from bone in pregnancy and lactation, Environmental Research, Vol. 92, Issue 2, June 2003, at http://www.sciencedirect.com/science/article/pii/S0013935103000203

 

98m1) Gulson et al., Mobilization of lead from the skeleton during the postnatal period is larger than during pregnancy. J Lab Clin Med 131:324-329 (1998).

98m2) Gulson et al., Mobilization of lead from human bone tissue during pregnancy and lactation--a summary of long-term research, Sci Total Environ, 2003 Feb 15;303(1-2):79-104. 

98n) Gulson et al., Blood Lead Changes during Pregnancy and Postpartum with Calcium Supplementation, Environmental Health Perspectives, Vol. 112, No. 15, Nov., 2004 at http://www.jstor.org/stable/3435607?seq=1#page_scan_tab_contents

 

98o)  Tellez-Rojo et al., Impact of Breastfeeding on the Mobilization of Lead from Bone, Am. J. Epidemiol.(2002) 155 (5): 420-428. doi: 10.1093/aje/155.5.420  at http://aje.oxfordjournals.org/content/155/5/420.full

-- The authors also refer to similar findings in Osterloh et al., Study of the effect of lactational bone loss on blood lead concentrations in humans. Env Health Perspect 1999;107:187–94.

 

98p) Goswami et al.,  Eye Cosmetic ‘Surma’: Hidden Threats of Lead Poisoning, Indian J Clin Biochem. 2013 Jan; 28(1): 71–73, Published online 2012 Aug 2. doi:  10.1007/s12291-012-0235-6, PMCID: PMC3547455, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3547455

 

98p1) From CDC document accessed in July, 2016:  Chapter 8. Management of Lead Hazards in the Environment of the Individual Child, Summary, at https://www.cdc.gov/nceh/lead/publications/books/plpyc/Chapter8.htm#Summary

 

98p2) CDC:  Guidelines for the Identification and Management of Lead Exposure in Pregnant and Lactating Women, National Center for Environmental Health/Agency for Toxic Substances and Disease Registry, 2010, p. 101, at http://www.cdc.gov/nceh/lead/publications/leadandpregnancy2010.pdf

 

98p3)  Tabatadze et al.,  Hair heavy metal and essential trace element concentration in children with autism spectrum disorder. Georgian Med News. <#> 2015 Nov;(248):77-82, at http://www.ncbi.nlm.nih.gov/pubmed/26656556

 

98q) Cecil et al., Decreased Brain Volume in Adults with Childhood Lead Exposure, PLOS / Medicine, May 27, 2008, at http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0050112

 

98q1)  CDC:  Guidelines for the Identification and Management of Lead Exposure in Pregnant and Lactating Women, National Center for Environmental Health/Agency for Toxic Substances and Disease Registry, 2010, at http://www.cdc.gov/nceh/lead/publications/leadandpregnancy2010.pdf

Ch. 9 (p. 97 ff.):  "Breastfeeding should continue for all infants with BLLs below 5 μg/dL or trending downward. "  "If ... infant BLL ≥5 μg/dL, then ... (steps should be taken) until maternal blood lead levels decline...."

 

98q2) Kim et al., Low-level lead exposure and autistic behaviors in school-age children, NeuroToxicology 53 (2016) 193–200, at http://www.ncbi.nlm.nih.gov/pubmed/26877220

 

98q3) Web page of Mayo clinic accessed July, 2016, at  http://www.mayoclinic.org/diseases-conditions/lead-poisoning/basics/definition/con-20035487

 

98q4) National Chart of Children <72 months Tested and Confirmed Elevated Blood Lead Level Rates by Year, linked at CDC web page on lead at https://www.cdc.gov/nceh/lead/data/national.htm

 

98q5) Huang et al., Childhood Blood Lead Levels and Symptoms of Attention Deficit Hyperactivity Disorder (ADHD): A Cross-Sectional Study of Mexican Children, Environ Health Perspect/; DOI:10.1289/ehp.1510067  Vol. 124, Issue 6, June, 2016, at http://ehp.niehs.nih.gov/15-10067/

 

98q6) Schnur et al., 2014, May, p. 240   Childhood lead poisoning and the new Centers for Disease Control and Prevention guidelines for lead exposure.  Journal of the American Association of Nurse Practitioners, 26(5), 238-247.

 

98q7) Pocock et al.,  Environmental lead and children's intelligence: a systematic review of the epidemiological evidence, BMJ 1994;309:1189 at http://www.bmj.com/content/309/6963/1189?

 

98q8) Al-Farsi et al., Levels of heavy metals and essential minerals in hair samples of children with autism in Oman: a case-control study, Biol Trace Elem Res. 2013 Feb;151(2):181-6. doi: 10.1007/s12011-012-9553-z. Epub 2012 Nov 28

 

98q9) Lakshmi Priya et al., Level of trace elements (copper, zinc, magnesium and selenium) and toxic elements (lead and mercury) in the hair and nail of children with autism, Biol Trace Elem Res. 2011 Aug;142(2):148-58. doi: 10.1007/s12011-010-8766-2. Epub 2010 Jul 13.

 

98q10) Fido et al., Toxic trace elements in the hair of children with autism, Autism, 2005 Jul;9(3):290-8.

 

98q11) Al-Ayadhi LY, Heavy metals and trace elements in hair samples of autistic children in central Saudi Arabia Neurosciences (Riyadh). 2005 Jul;10(3):213-8.

 

98q12) Blaurock-Busch et al., Toxic Metals and Essential Elements in Hair and Severity of Symptoms among Children with Autism,  Maedica (Buchar). 2012 Jan;7(1):38-48. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3484795/

98q13)  Blaurock-Busch et al., Heavy metals and trace elements in hair and urine of a sample of arab children with autistic spectrum disorder,Maedica (Buchar). 2011 Oct;6(4):247-57.

98q14) Bellinger and Needleman, Intellectual Impairment and Blood Lead Levels, N Engl J Med 2003; 349:500-502July 31, 2003, at http://www.nejm.org/doi/full/10.1056/NEJM200307313490515

98q15) Braun et al., Exposures to Environmental Toxicants and Attention Deficit Hyperactivity Disorder in U.S. Children, Environ Health Perspect <#>. 2006 Dec; 114(12): at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1764142

 

98q16) Daneshparvar et al., The Role of Lead Exposure on Attention-Deficit/ Hyperactivity Disorder ‎in Children: A Systematic Review, Iran J Psychiatry, v.11(1); 2016 Jan, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888135/ 

 

98q17)  Adams and 12 others, The Severity of Autism Is Associated with Toxic Metal Body Burden and Red Blood Cell Glutathione Levels, J Toxicol v.2009; 2009 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2809421/

 

98q18) Nigg et al., Confirmation and extension of association of blood lead with attention-deficit/hyperactivity disorder (ADHD) and ADHD symptom domains at population-typical exposure levels, J Child Psychol Psychiatry.  2010 Jan;51(1):58-65. at https://www.ncbi.nlm.nih.gov/pubmed/19941632

 

98q19) Mohamed et al.,  Sample of Autistic Egyptian Children: Environmental Risk Factors of Heavy Metals in Autism, Behavioural Neurology, Volume 2015 (2015), Article ID 545674, https://www.hindawi.com/journals/bn/2015/545674/abs/

 

98q20)  Ha et al., Low blood levels of lead and mercury and symptoms of attention deficit hyperactivity in children: a report of the children's health and environment research (CHEER), Neurotoxicology, Jan 2009, at https://www.ncbi.nlm.nih.gov/pubmed/19100765/

 

98r) Nordin et al., Prevalence of excess lead absorption and associated risk factors in children enrolled in a midwestern health maintenance organization, Pediatrics, 1994 Feb;93(2):172-7, at http://www.ncbi.nlm.nih.gov/pubmed/8121726.  Elevated blood levels were found to be three to eight times as numerous as measured in urban clinics compared with suburban clinics, in Minnesota, USA.

 

98s)  Muldoon et al., Lifestyle and Sociodemographic Factors as Determinants of Blood Lead Levels in Elderly Women, Am. J. Epidemiol. I, 1994 139 (6), p. 599,  Table 2, abstract at http://aje.oxfordjournals.org/content/139/6/599.abstract.  The 11% reduction comes from dividing the average difference between the blood levels of women who had breastfed and the blood levels of women who had not breastfed (0.59 mcg -- see Table 2) by the 5.4 mcg average blood levels.

 

98t) Kessler, Sunset for Leaded Aviation Gasoline?  Environmental Health Perspectives, accessed July 2016, at http://ehp.niehs.nih.gov/121-a54/

 

98u) Tong et al., Environmental lead exposure: a public health problem of global dimensions,  Bull World Health Organ vol.78 n.9 Genebra Jan. 2000, at http://www.scielosp.org/scielo.php?script=sci_arttext&pid=S0042-96862000000900003

 

98u1) FDA web page on lead at http://www.fda.gov/Food/FoodborneIllnessContaminants/Metals/ucm233520.htm

 

98u2) Kot et al., Assessment of cadmium contamination in cereals, cereal products and potatoes. Bromat Chem Toksykol. 2009;3:537–542

 

98v) EPA web page at https://www.epa.gov/ground-water-and-drinking-water/table-regulated-drinking-water-contaminants

 

98w) WHO:  Minor and Trace Elements in Breast Milk, Report of a Joint WHO/IAEA Collaborative Study, Geneva, 1989

 

98x) U.S. CDC:  Guidelines for the identification and management of lead exposure in pregnant and lactating women, Nov. 2010, p. 35, at www.cdc.gov/nceh/lead/publications/leadandpregnancy2010.pdf

 

98y) EPA website at https://www.epa.gov/sites/production/files/2015-10/documents/ace3_neurodevelopmental.pdf, p. 7.

 

98z) CDC web page at http://www.cdc.gov/nceh/lead/data/index.htm

 

98z1) Miranda et al., The Relationship between Early Childhood Blood Lead Levels and Performance on End-of-Grade Tests, Environ Health Perspect, 2007 Aug; 115(8): 1242–1247. at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940087/

 

98z2)  Hong et al., Environmental Lead Exposure and Attention Deficit/Hyperactivity Disorder Symptom Domains in a Community Sample of South Korean School-Age Children, Environ Health Perspect 2015 Mar; 123(3): 271–276. at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4348739/

 

98z3)  Schwartz, J:  Low-Level Lead Exposure and Children′s IQ: A Metaanalysis and Search for a Threshold, Environmental Research, Volume 65, Issue 1, April 1994, Pages 42-55, at http://www.sciencedirect.com/science/article/pii/S0013935184710206

98z4)  Health Canada:  Final Human Health State of the Science Report on Lead, at http://www.hc-sc.gc.ca/ewh-semt/pubs/contaminants/dhhssrl-rpecscepsh/index-eng.php#a91, accessed August, 2016.

99) Summary Health Statistics for U.S. Children: National Health Interview Survey, 2012, Appendix III, table VI, at http://www.cdc.gov/nchs/data/series/sr_10/sr10_258.pdf

 

99a) Figure 4 in CDC, Vital and Health Statistics, July 2008, Diagnosed Attention Deficit Hyperactivity Disorder and Learning Disability: United States, 2004–2006  at www.cdc.gov/nchs/data/series/sr_10/Sr10_237.pdf, is just a small part of the evidence, for a generalization that is basically general knowledge.

 

99b) Judy L. Cameron, Dept. of Psychiatry, Neuroscience, and Cell Biology and Physiology, University of Pittsburgh, in "Effects of Sex Hormones on Brain Development," Chapter 5 of Handbook of Developmental Cognitive Neuroscience, MIT Press, 2001, edited by Charles A. Nelson and Monica Luciana. Charles A. Nelson is Research Director, Developmental Medicine Center at Children's Hospital Boston, and Professor of Pediatrics and Richard David Scott Chair in Pediatric Developmental Medicine Research at Harvard Medical School. Selected pages can be found at no charge at http://www.worldcat.org/title/handbook-of-developmental-cognitive-neuroscience/oclc/45059115/viewport or at worldcat.org’s website, doing a search including the above book title and “sex steroids.”

 

99c)  McEwen, Steroid Hormones and Brain Development: Some Guidelines for Understanding Actions of Pseudohormones and Other Toxic Agents, Environmental Health Perspectives Vol. 74, pp. 177-184, 1987.

 

99d) at http://www.amazon.com/Boys-Adrift-Epidemic-Unmotivated-Underachieving/dp/0465072100

 

99e) at http://www.theatlantic.com/education/archive/2013/09/how-to-make-school-better-for-boys/279635/

 

99f) Richard Whitmire, Why Boys Fail: Saving Our Sons from an Educational System That's Leaving Them Behind,  AMACOM. “…why so many boys arrive in twelfth grade unprepared for college work and why so many young men who do go to college drop out before earning degrees. Is it really because classrooms are feminized? Is it really because their minds were warped by video games? Is it really because mothers cut the apron strings prematurely?”  also, “the oppressive boy code and guy code,” and “the feminist-dominated teaching profession.”

 

99g) Is the gender gap in higher education widening?  by Dirk Van Damme, Head of the Innovation and Measuring Division, Directorate for

Education and Skills, at http://oecdeducationtoday.blogspot.com/2016/01/is-gender-gap-in-higher-education.html, Monday, January 11, 2016

 

99h) Tamar Lewin: At Colleges, Women Are Leaving Men in the Dust, New York Times, July 9, 2006  at http://www.nytimes.com/2006/07/09/education/09college.html?pagewanted=all

Quoting from that article:  “the gender gap has moved to the front burner in part because of interest from educated mothers worrying that their sons are adrift now that it's a problem of white sons of college-educated parents.” The sociodemographic groups with the highest rates of breastfeeding are whites and college graduates.

 

99k) The weaker sex:  Boys are being outclassed by girls at both school and university, and the gap is widening, The Economist, Mar 7th 2015, at http://www.economist.com/news/international/21645759-boys-are-being-outclassed-girls-both-school-and-university-and-gap

 

99m) Christina Hoff Sommers, The War Against Boys:  How Misguided Feminism Is Harming Our Young Men (2000) Simon & Schuster, Chapter 1, at https://www.nytimes.com/books/first/s/sommers-war.html

 

99n)

http://www.pollution-effects.info/index_files/image017.gif

 


99o) Colciago et al., Chronic treatment with polychlorinated biphenyls (PCB) during pregnancy and lactation in the rat, Part 2, Toxicology and Applied Pharmacology, May 2009, at http://www.ncbi.nlm.nih.gov/pubmed/19464308

 

99o1) Sobolewski et al., Sex-specific enhanced behavioral toxicity induced by maternal exposure to a mixture of low dose endocrine-disrupting chemicals, Neurotoxicology, 2014 Dec;45:121-30. doi: 10.1016/j.neuro.2014.09.008. Epub 2014 Oct 22, at http://www.ncbi.nlm.nih.gov/pubmed/25454719

 

99p) Coccini et al., Perinatal co-exposure to methylmercury and PCB153 or PCB126 in rats alters the cerebral cholinergic muscarinic receptors at weaning and puberty, Toxicology, 2007 Aug 16;238(1):34-48. Epub 2007 May 25, at https://www.ncbi.nlm.nih.gov/pubmed/17618726

 

99r) Nguon et al., Perinatal exposure to polychlorinated biphenyls differentially affects cerebellar development and motor functions in male and female rat neonates, The Cerebellum, June 2005, Volume 4, Issue 2, at http://link.springer.com/article/10.1080/14734220510007860#/page-1

 

99s) Onishchenko et al., Developmental Exposure to Methylmercury Alters Learning and Induces Depression-like Behavior in Male Mice, Toxicological Sciences, Vol. 150, Issue 2, April 2016, at http://toxsci.oxfordjournals.org/content/97/2/428

 

99t) Liu et al., Adverse Associations of both Prenatal and Postnatal Exposure to Organophosphorous Pesticides with Infant Neurodevelopment in an Agricultural Area of Jiangsu Province, China, Environ Health Perspect, May, 2016,  DOI: 10.1289/EHP196, at http://ehp.niehs.nih.gov/EHP196/

 

99u) See www.air-pollution-autism.info, Sections 3.c and 3.d)

 

99v) Pesticides in the Diets of Infants and Children, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C.  1993, p. 43 at http://www.nap.edu/openbook.php?record_id=2126&page=43 

 

99w) Wagner-Schuman et al., Association of pyrethroid pesticide exposure with attention-deficit/hyperactivity disorder in a nationally representative sample of U.S. children, Environ Health, v.14; 2015 at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458051/

 

99x) Li et al., Breastfeeding Rates in the United States by Characteristics of the Child, Mother, or Family:  The 2002 National Immunization Survey, Pediatrics, Jan. 2005, Vol. 115, Issue 1, Fig. 1 (from 2002 NIS) at http://pediatrics.aappublications.org/content/115/1/e31

 

100) P. Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants,  Environmental Health Perspectives, accepted Oct. 1993   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1567218/pdf 

 

101) 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 http://www.ncbi.nlm.nih.gov/pubmed/17237965

This study found that mercury measured in infants’ hair increased 446% during the first six months of breastfeeding, while mercury measured in the mothers’ hair decreased 57%. These measurements included mercury from vaccines (still containing mercury at that time in Brazil, where the study was carried out), which the authors estimated accounted for about 40% of the infants’ exposure during those six months.  Given that, combined with the finding in the Chien et al. study that over 95% of an infant’s exposure to mercury was from breastfeeding,96 the increase in the infants’ mercury levels attributable to breastfeeding was probably well over 100% during the first 6 months of breastfeeding.

 

101a)  Byczkowski et al., 'Occupational' exposure of infants to toxic chemicals via breast milk, Nutrition · January 1994, at https://www.researchgate.net/publication/15000689_%27Occupational%27_exposure_of_infants_to_toxic_chemicals_via_breast_milk , citing Gonzales et al., Mercury in human hair: a study of residents in Madrid, Spain, Arch, Environm Health 1985;40,225

 

102) Stephen B. Klein and B. Michael Thorne in their Biological Psychology (2006), Worth Publishers, p. 390

 See also Sex matters in autism and other developmental disabilities, Thompson, Caruso and  Nellerbeck, Journal of Learning Disabilities, p. 352, referring to COLLAER, M. L. & HINES, M.  ‘Human Behavioral Sex Differences: A Role for Gonadal Hormones during Early Development?’, Psychological Bulletin

 

103a) Quoted from WebMD web page at http://www.webmd.com/men/features/how-low-testosterone-affects-your-health?page=2

 

103b) See Table 1b of Bhasin et al., Testosterone Therapy in Adult Men with Androgen Deficiency Syndromes:  An Endocrine Society Clinical Practice Guideline, The Journal of Clinical Endocrinology & Metabolism, Volume 91, Issue 6, First Published Online: July 02, 2013. At http://press.endocrine.org/doi/full/10.1210/jc.2005-2847

 

103c)  R.J. Andrew: Testosterone, attention and memory, Conclusion of chapter 7, p. 186, in Patrick Bateson, Ed., The Development and Integration of Behaviour, 1991, Cambridge University Press,  which can probably be found on Google by doing a search for “testosterone effect on motivation concentration attention”  possibly at

 https://books.google.com/books?hl=en&lr=&id=Q2E6IC2PhSYC&oi=fnd&pg=PA171&dq=testosterone+effect+on+motivation+concentration+attention&ots=33tYd8dtS1&sig=c05FGCUd72RPjlKWcLfhRRXY-PA#v=onepage&q=testosterone%20effect%20on%20motivation%20concentration%20attention&f=false

 

103d)  Lesmana et al., Lactational exposure to hydroxylated polychlorinated biphenyl (OH-PCB 106) causes hyperactivity in male rat pups by aberrant increase in dopamine and its receptor, Environ Toxicol,2014 Aug;29(8):876-83. doi: 10.1002/tox.21815. Epub 2012 Sep 20, at https://www.ncbi.nlm.nih.gov/pubmed/22996836

 

103e) Shakkebaek et al., Male Reproductive Disorders and Fertility Trends: Influences of Environment and Genetic Susceptibility, Physiol Rev. <#> 2016 Jan;96(1):55-97. doi: 10.1152/physrev.00017.2015, at http://www.ncbi.nlm.nih.gov/pubmed/26582516 

 

103f) from a web page of American Physiological Society: at http://www.the-aps.org/mm/hp/Audiences/Public-Press/2015-68.html

 

103g) Sharpe, RM 2010, 'Environmental/lifestyle effects on spermatogenesis' Philosophical Transactions of the Royal Society B: Biological Sciences, vol 365, no. 1546, pp. 1697-1712., 10.1098/rstb.2009.0206 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2871918/

 

103h) Auyeung et al., Prenatal and postnatal hormone effects on the human brain and cognition, Pflugers Arch - Eur J Physiol, 2013, at http://docs.autismresearchcentre.com/papers/2013_Auyeung_Prenatal%20and%20postnatal%20hormone%20effects_EuJPhysio.pdf

 

103k) Berensztein et al., Apoptosis and proliferation of human testicular somatic and germ cells during prepuberty: high rate of testicular growth in newborns mediated by decreased apoptosis. J Clin Endocrinol Metab. 2002;87:5113–8.

 

103m) MacLeod et al., Androgen action in the masculinization programming window and development of male reproductive organs, Int J Androl. 2010 Apr;33(2):279-87. at http://www.ncbi.nlm.nih.gov/pubmed/20002220

 

104) U.S. CDC:  Biomonitoring Summary, Dioxin-Like Chemicals: Polychlorinated Dibenzo-/p/-dioxins, Polychlorinated Dibenzofurans, and Coplanar and  Mono-/ortho/-substituted Polychlorinated Biphenyls, at http://www.cdc.gov/biomonitoring/DioxinLikeChemicals_BiomonitoringSummary.html 

 

105)  Environmental Endocrine Disruption:  An Effects Assessment and Analysis, by Thomas Crisp and 12 other researchers with the EPA,  in Environmental Health Perspectives, Vol. 106, Feb. 1998, Supplement. P. 27 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1533291/pdf/envhper00536-0026.pdf

 

106a) Meeker et al., Exposure to polychlorinated biphenyls (PCBs) and male reproduction, Syst Biol Reprod Med. <#> 2010 Apr;56(2):122-31. doi:10.3109/19396360903443658, at http://www.ncbi.nlm.nih.gov/pubmed/20377311

 

106b) Medical Dictionary for the Health Professions and Nursing © Farlex 2012

 

106c) Kaya et al., Mixture of Polychlorinated Biphenyls on Sex-Dependent Behaviors and Steroid Hormone Concentrations in Rats: Dose–Response Relationship, Toxicology and Applied Pharmacology , Jan. 2002, at http://www.ncbi.nlm.nih.gov/pubmed/11814327

Female rats were exposed to a mixture of PCBs that was similar in composition to that in human breast milk, beginning before mating and continuing to the day of birth of the subsequent litter. At birth, concentrations of PCBs in the brains of the offspring were much lower than in the mother rats; but after weaning, PCB levels in the offsprings’ brains ranged from two-and-a-half to five times the levels in the brains of the dams.(Bear in mind that this degree of concentrating of the toxin as part of lactational transfer to the infants is what happens when maternal toxins are shared among an entire litter of infants.) 

 

106d) Schell et al., Relationships of Polychlorinated Biphenyls and Dichlorodiphenyldichloroethylene (/p,p’/-DDE) with Testosterone Levels in Adolescent Males, Environ Health Perspect v.122(3); 2014 Mar, PMC3948020, Table 2, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3948020

 

106e) Needham et al., Assessing Developmental Toxicant Exposures via Biomonitoring,  Basic & Clinical Pharmacology & Toxicology Doi: 10.1111/j.1742-7843.2007.00185.x, p. 106  at http://onlinelibrary.wiley.com/doi/10.1111/j.1742-7843.2007.00185.x/epdf

 

106f) Schell et al., Organochlorines, Lead, and Mercury in Akwesasne Mohawk Youth, Volume 111 | Number 7 | June 2003 • Environmental Health Perspectives, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241531/pdf/ehp0111-000954.pdf

                                                                           

107)  Costa and Giordano, Developmental Neurotoxicity Of Polybrominated Diphenyl Ether (PBDE) Flame Retardants,  2008  Neurotoxicology   National Center for Biotechnology Information,  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052/

 

108) Kuriyama et al., Developmental exposure to low dose PBDE 99: effects on male fertility and neurobehavior in rat offspring, Environ Health Perspect. 2005 Feb; 113(2):149-54at http://www.ncbi.nlm.nih.gov/pubmed/15687051

 

108a) CDC, Vital and Health Statistics, July 2008, Diagnosed Attention Deficit Hyperactivity Disorder and Learning Disability: United States, 2004–2006  at www.cdc.gov/nchs/data/series/sr_10/Sr10_237.pdf, p. 7

 

109) Medscape web page on estradiol by Alina G Sofronescu, PhD; Chief Editor: Eric B Staros, MD, at http://emedicine.medscape.com/article/2089003-overview

 

110) M.M. McCarthy, The Two Faces of Estradiol, Effects on the Developing Brain, Neuroscientist, 2009, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2795061/

 

111) Gillies, Estrogen Actions in the Brain and the Basis for Differential Action in Men and Women: A Case for Sex-Specific Medicines, Pharmacol Rev. 2010 Jun; 62(2): 155–198, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879914/

 

112)  Oregon Department of Environmental Quality Environmental Cleanup Program, Oct. 2010, 10-LQ-023, p. D2-4 (near very end) at http://www.deq.state.or.us/lq/pubs/docs/cu/HumanHealthRiskAssessmentGuidance.pdf  “The doses of PCBs that a breastfeeding infant may be expected to receive, given breast milk PCB concentrations measured in the literature, are presented in table 1. These doses range from 0.0019 to 0.0081 mg/kg/day and are 63-270 times higher than ATSDR’s minimal risk level (0.00003 mg/kg/day) for PCB exposures that last between 15 and 364 days.”

 

112a) Exhibit 2-2 of National Longitudinal Transitional Study 2:  Youth with Disabilities: A Changing Population, Prepared for Office of Special Education Programs, U.S. Dept. of Education, at http://www.nlts2.org/reports/2003_04-1/index.html, then selecting and viewing Chapter 2, on p. 2-3: The gender distribution of youth with disabilities did not change significantly over time (69% and 67% male, Exhibit 2-2).”

 

112b) R.M.Sharpe, Environmental/lifestyle effects on spermatogenesis, Philos Trans R Soc Lond B Biol Sci. 2010 May 27; 365(1546): 1697–1712. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2871918/

 

112c) Bjorling-Poulsen et al., Potential developmental neurotoxicity of pesticides used in Europe, Environ Health. 2008; 7: 50. PMCID: PMC2577708  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577708/ 

 

113) 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/

 

113a) See Section A and Section B.2 of www.child-disability.info.   

 

114) Houtrow et al., Changing Trends of Childhood Disability, 2001–2011, Pediatrics Vol. 134 No. 3 September 1, 2014 at http://pediatrics.aappublications.org/content/134/3/530.abstract

 

114a) at  http://nlts2.org/reports/2003_04-1/nlts2_report_2003_04-1_complete.pdf, Exhibit 2-1.

 

114b) U.S. CDC, National Vital Statistics Reports, Vol. 50, No. 5, Table 1,

at http://www.cdc.gov/nchs/data/nvsr/nvsr50/nvsr50_05.pdf, adding up the total births during each of the three-year periods (1970-72 and 1984-86) that would have applied to 15-17-year-olds in 1987 and 2001, and dividing the latter by the former.

 

114c)  G. Reid Lyon, Learning Disabilities, The Future of Children, Vol. 6, No. 1, Special Education for Students with Disabilities (Spring, 1996), pp. 54-76 DOI: 10.2307/1602494 at http://www.jstor.org/stable/1602494

 

114d)  Brominated Flame Retardants, Third annual report to the Maine Legislature, Jan. 2007, Maine Dept. of Environmental Protection, Maine Center for Disease Control and Prevention, Dr. Deborah Rice et al., at http://www.maine.gov/dep/waste/publications/legislativereports/documents/finalrptjan07.pdf

 

114e) Drotar, reviewing:  A Young Mind in a Growing Brain (by Kagan and Herschkowitz, 2005); the review is in Journal of Developmental & Behavioral Pediatrics,:February 2007 - Volume 28 - Issue 1 - p 79 at http://journals.lww.com/jrnldbp/pages/articleviewer.aspx?year=2007&issue=02000&article=00022&type=Fulltext

 

114f) Petanjek et al., Lifespan Alteration of Basal Dendritic Trees of Pyramidal Neurons in the Human Prefrontal Cortex:  A Layer-Specific Pattern,   Cerebral Cortex, April 2008, at http://cercor.oxfordjournals.org/content/18/4/915.full.pdf+html

 

114g)  Shazia et al., Neuropsychology of prefrontal cortex, Indian J Psychiatry, v.50(3); Jul-Sep 2008 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738354/

 

114h) Holland et al., Structural Growth Trajectories and Rates of Change in the First 3 Months of Infant Brain Development, JAMA Neurol. 2014 Oct; 71(10): 1266–1274. at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4940157/

 

114j) Elston et al., The Pyramidal Cell in Cognition: A Comparative Study in Human and Monkey, Journal of Neuroscience, 2001, Vol. 21, at http://www.jneurosci.org/content/21/17/RC163.full.pdf

 

115) Exhibit 2-1 of National Longitudinal Transitional Study 2:  Youth with Disabilities: A Changing Population, Prepared for Office of Special Education Programs, U.S. Dept. of Education, at http://nlts2.org/reports/2003_04-1/nlts2_report_2003_04-1complete.pdf

 

116) Shamberger, R.J., Autism rates associated with nutrition and the WIC program, J Am Coll Nutr. 2011 Oct;30(5):348-53.  Abstract at www.ncbi.nlm.nih.gov/pubmed/22081621

 

117) 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   This 2010 Canadian study, drawing data from a population-based clinically-rich perinatal database,” investigated a very large population, nearly 130,000 births.  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. 

 

118) Whitely et al., Trends in Developmental, Behavioral and Somatic Factors by Diagnostic Sub-group in Pervasive Developmental Disorders: A Follow-up Analysis, pp. 10, 14  Autism Insights 2009:1 3-17  at https://www.academia.edu/17814363/Trends_in_Developmental_Behavioral_and_somatic_Factors_by_Diagnostic_sub-group_in_pervasive_Developmental_Disorders_A_Follow-up_AnalysisThis study found that 65% of autism cases had been breastfed for at least four weeks; the authors 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 would apply for the equivalent period (just after four weeks). That is also as was found in the U.K. Infant Feeding Survey - UK, 2010 Publication date: November 20, 2012, Chapter 2, at http://www.hscic.gov.uk/catalogue/PUB08694/ifs-uk-2010-chap2-inc-prev-dur.pdf

 

119)  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  https://imfar.confex.com/imfar/2010/webprogram/Paper6362.html)   Thi