http://www.pollution-effects.info/index_files/image001.gif­ 

 

 

Some Effects of Environmental Pollution on Development of Infants

 

Summary

 

Section 1.

Section 1.a (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.  Toxins present in food are a very important form of such exposure.  (The full text, including references to authoritative sources, is in Section 1.a)

 

Section 1.b (summary)There were huge increases in numbers and quantities of chemicals after World War II, which have resulted in major increases in toxic pollutants in human environments since that time.  According to experts writing in 2004, "these substances have caused contamination of human milk only during the last half century, and long-term health impacts are now being discovered."6b (The full text, including references to authoritative sources, is in Section 1.b)

 

Section 2

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

 

http://www.pollution-effects.info/index_files/image002.gif
 

 

(Section 2 summary, cont.) 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, due to the placental barrier and to concentration via the process of lactation:

 

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)   The State of Washington Department of Ecology considers breastfed infants to be at the very highest level of exposure to common environmental 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 the Section 3 Introduction)

 

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)

http://www.pollution-effects.info/index_files/image004.gif


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)

 

 

Section  3.a.2Lactational transfer of PCBs to infants:  Exposures to PCBs after birth are likely to be far higher than before birth, especially with breastfeeding for a few months or more.

 

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.2)

 

Substantial evidence also indicates that, following developmental exposure to PCBs (and other toxins discussed here), adverse effects are often only found well past early childhood.  This will be discussed in Section 3.f

 

 

 

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):  Dioxins, according to a major toxicology textbook, 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 several months 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.  According to impeccable authority, "No amount of lead exposure is safe."

 

Associations have been found in many studies between autism and heavy metal (lead and mercury) exposure at levels often occurring in developed countries.  Many studies have also found associations closely linking ADHD with such lead exposures.

(Link to full text, with citations of authoritative sources, at Section 3.e)

 

 

Section 3.f: (Summary)  These toxins are known to often have effects that are apparent in later childhood and/or adulthood, while not being noticed earlier.  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 this section 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.   3.f

 

Section 3.g (Summary):  All of the above toxins have been found to be present in human milk in concentrations either exceeding established safe levels (in four cases) or in substantial amounts (in two cases), and their combined effects are likely to be more than merely additive. Details and citations of sources in the subsections of Section 3.

 

  

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

 Section 4.a.1: (Summary):   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:  (Summary):  Emissions from municipal incinerators were found to be closely associated with all of the autism-related outcomes that were investigated in children who had been breastfed; on the other hand, effects of those emissions as found in children in the general population were far smaller.  (Full text at Section 4.a.2.1)

 

Section 4.a.2.2. (a) Fairly common pesticide exposures are closely linked with autism risk, in many studies;  

 

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

 

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

. (Full text, including references to authoritative sources, at Section 4.a.2.2)

 

 

Section 4.a.2.3:  (Summary):  Exposures to airborne toxins in the first year after birth have been found to be strongly associated with risk of autism. Logically implicated toxins are taken in by infants far more via breastfeeding than by other pathways. (Full text at Section (Summary):

4.a.2.3)

 

 

Section 4.b:  (Summary):  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.

 

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.

  Preview of Fig. 6.a

http://www.pollution-effects.info/index_files/image025.gif
 

 

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, considering that several toxins are present in human milk in concentrations far in excess of established safe levels.  (Full text, including references to sources, at Section 4.b)

 

Section 4.c:  (Summary):  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.

 

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.  Looking back at when the boys would have been infants who would have been the first to widely have these problems as they grew older, one can see the mid-to-late 1970’s as the likely birth years of the boys and young men who would later have been the first ones having the problems of concern here.  Breastfeeding rates were very rapidly increasing during that period; human milk is clearly a major source of infant exposure to developmental toxins from the environment (see Section 3).  Apparently nobody knows about existence of any other major pathway for developmental toxins to infants in doses exceeding established safe levels. (see Section 6).  And authoritative testing has found little or none of those chemicals in contemporary infant formula in the U.S. (see Sections 3 and 8)

 

Section 8: (summary):  

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. Human milk has been found to normally contain many pesticides, and infant formula in the U.S. has been found to contain essentially none. Exposures of children to pesticides at current background levels correlate well with reduced mental capacities as well as with ASD, ADHD, and other neurodevelopmental problems, in many studies. 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, including in concentrated doses. (For a more complete summary, with link to the full text on this topic, go to Section 8.)

 

 

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

 

image031.gif

 

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

  

(Section 9 summary, cont.)  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:  (summary):  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):  Promoters of breastfeeding base their case almost entirely on observational studies and on outcomes assessed in early childhood.  There are fundamental weaknesses in observational studies, as recognized by experts on medical evidence; and there are excellent reasons to pay far more attention to long-term outcomes. For details and authoritative sources, see Section 10.

 

Section 11:  (summary):  Promotion of breastfeeding is based mainly on observations of what appear to be short-term benefits; the evidence about longer-term effects strongly indicates worse long-term health outcomes.  (For full text including citations of authoritative sources, see Section 11.)

 

Section 12:  (summary):  Randomized trials are recognized as being far superior to observational studies.  The few randomized trials that have dealt with breastfeeding have shown revealing results.  (For details, see Section 12.)

 

Section 13 (summary): Final remarks

Section 13.a:  (summary):  A reasonable question to consider: 

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 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 large number 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)

 

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

 

 Section 13.b: (summary):   A viable alternative to breastfeeding:

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 13b)

 

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

Section 1.a:  Substantial increases in major non-communicable 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 13 that points to this same time of transition to declining child health (see Trend....).

 

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 1.b:  Substantial increases in toxic chemicals in human environments beginning after World War II: 

 

As of the 1940's, relatively few environmental chemicals were recognized as being hazards to the growing child.  It was after World War II that chemicals developed during the war were modified for use as pesticides and for other common uses and were produced in increasing numbers.6a, 6c  According to data from the American Chemical Society, production of chemicals increased over 350% in the 25 years after 1947, compared with an 85% increase during the next 24 years.6d  Referring to specific types of chemicals that are of special concern for child development, researchers who are authors or co-authors of over 340 studies have stated, "It is now recognized that numerous endocrine-disrupting chemicals have been released into the environment in large quantities since World War II;" among other chemicals the authors listed in this category were many pesticides and PCBs, dioxins, and mercury. 6c

 

Speaking in broad terms, experts on the subject of environmental toxins 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."6b

 

 

Section 2: 

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

 

There is a widespread belief that postnatal exposures to developmental toxins are of only minor significance in comparison with prenatal exposures, but there is ample evidence indicating that such a notion is misguided. 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 developmental processes represented.)  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 times 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.)

 

 

http://www.pollution-effects.info/index_files/image003.gif

  

 
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 are far greater postnatally than prenatally, due to the placental barrier before birth and to concentration via lactation after birth:

 

An official book of the American Academy of Pediatrics stated in 2012 that "the relatively high concentration of fat in human milk means that fat-soluble substances will, in effect, concentrate there." (Fat-soluble substances that were being discussed included PCB, PBDEs and various pesticides.)24b  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

 

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  One study, by a research team who are authors or coauthors of well over 1000 studies, estimated PBDE intake from food to be 307 ng/kg/day for nursing infants compared with 0.9 ng/kg/day in adult females.18d   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)   In a study cited by the ATSDR, it was found that at 11 months of age, dioxin toxicity-equivalent concentrations in infants who had been breastfed 6-7 months were about 10 times those in formula-fed infants; dioxin levels in breastfed infants were still an average of about 2.5 times the maternal values, months after the average breastfeeding had ended. 79  Considerable other evidence can be found in Appendix G concerning lactation's property of concentrating toxins in the process of transferring them to infants.

 

 

Section 2.c:  The vulnerability to developmental toxins of concern here is to toxins that most infants are exposed to, 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, 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 Another study team calculated that 91% of a typical U.S. breastfed infant’s total exposure to PBDEs was from breast milk.56e Those are examples of data that help form expert generalizations such as stated above in Section 2.b, indicating major concentration of environmental toxins taking place via the process of lactation.  

  

 

The end result of infants' being exposed to toxins either directly or 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 earliest months after birth are likely to be the period most vulnerable to developmental toxins, for various reasons:

 

--  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 

-- 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

-- Overall growth of the brain is unusually rapid in the early weeks after birth (1% per day at first, declining to 0.4% per day after 3 months).114h  Remember from Section 2.a about heightened vulnerability of neurological development during rapid growth of the brain. 

-- The type of dioxin that is the predominant type in human milk (OCDD) declines in its concentration in breast milk by 50% during the first month after birth,93d which is in line with long-term maternal accumulations of this toxin being excreted in the milk.85 

-- Showing similar presence of maximum concentrations of developmental toxins during the first month(s) after birth, lactating mothers' blood levels of mercury were found to decline by 70% during the first two months after birth.84,

-- A web page of the NIH states that neonatal hypothyroidism, which it says can cause intellectual disability, can result from thyroid levels that are “only slightly low.”93e (“Neonatal” refers to the first four weeks after birth.)  Note that thyroid levels are known to be reduced by toxins including dioxins,93g PCBs,93h and PBDEs93j all of which are substantially present in breast milk; dioxins are present in breast milk in especially high concentrations in the early weeks after birth.73a, 93d Several other authoritative sources concur with the statement of serious consequences of neonatal hypothyroidism, including statements in an Oxford Journal about “devastating functional consequences” and “mental retardation resulting from neonatal thyroid hormone deficiency.”93f,

--  For substantial additional evidence of special vulnerability of neurological development during the first 3 to 4 weeks after birth, including an aspect of development of the autism-related cerebellum, see Section 2.a of www.air-pollution-autism.info

--  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. 

--  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.

--  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

 --  Also see below for additional evidence on this topic, specifically showing vulnerability to PCBs in the first two to three months after birth.

 

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:

 

Four studies since 2009 that have found direct associations between autism and a distinctly postnatal exposure (breastfeeding) will be described in 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.”   In addition, studies will be described showing indirect associations between breastfeeding and autism, in which (a) the breastfeeding-associated outcome is characteristics that are known traits of autism, and (b) breastfeeding is the predominant pathway to infants of a substance (pesticides), exposure to which is known to be very closely linked with 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:

 

Introduction:

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” (PBTs), 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 (developing children) that isparticularly vulnerable to disruptive toxins such as PCBs, PBDEs, dioxins, and "metals of concern;"

  (b) within that particularly vulnerable larger group, there is a smaller subgroup that has greater sensitivity:  the infant age group; 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 an adult,24a the average daily PCB intake of a breastfed infant per kg of body weight has been found to be 150 times that of an adult,18a and PBDE intake from human milk has been authoritatively estimated to be over 300 times higher than that of a typical adult female.18d  And according to the American Academy of Pediatrics in 2012, referring specifically to PCBs, PBDEs, and major types of pesticides, "Infant formula is free of these residues, because the lipid comes from coconuts or other sources low on the food chain."24b

 

……………………..

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 and Section 4.a.2.1).  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 other adverse neurological effects of PCBs.

 

 

Early higher exposures:  During the period of especially high developmental vulnerability (see Section 2.d) 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 Section 2.b); also see the charts (Figure 4) 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.a 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.  While discussing effects of PCBs other than on IQ and memory, note that a research team cited nine studies to support its statement about "chronic effects (of PCBs) on a range of social and anxiety-related behaviors." 23a

 Fig. 4

PCBs in relation to breastfeeding and infant formula  

Section 3.a.2:  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 15 different 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 toxicity of its "Developmental Effects."

 

Adverse exposures to PCBs are not limited to an insignificant minority.  According to a research team who are authors or co-authors of over 340 scientific studies among them, writing in 1993, "Based on current breast milk concentrations nationwide, it is estimated that at least 5% and possibly more of the babies born in the United States are exposed to quantities of PCBs sufficient to cause neurological effects."6c That was published in a year when breastfeeding for six months was half of its current rate. (see Figure 7)  PCBs in the environment may have declined since 1993, but comparably toxic chemical relatives of PCBs have greatly increased in the environment since that time. (see Merzenich quote below and also Section 3.b)

 

  

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 the 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 also pointed out that, as a result of the PCB exposures, "the brain remained into adulthood in a very primitive underdeveloped state."  And he stated 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.36  According to a consensus statement signed by 57 scientists, researchers and health professionals, including many who are highly published experts, "The concordance between human and animal neurotoxicity assessment is remarkable as demonstrated for lead, mercury and PCBs."36a

 

Given the above, note that several epidemiological studies have found breastfeeding duration to be associated with autism prevalence, including in dose-response relationships.  Those will be described in Section 4.

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

 

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 auditory impairment in those with autism, it should not be surprising that difficulties in communicating are a basic characteristic of autism.  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.

 

 

To see good 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   

 

 

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 at www.male-development.info about the strong negative effect on learning ability that has been found to result from PCB exposure, in an animal experiment.  The harm to learning ability resulting from PCB exposure as seen in that experiment was major, even though damage by PCBs to hearing ability would not have contributed to the lack of learning in that case, as it would with humans.

 

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 some cases, but (by ignoring the huge differences in those exposures depending on source) they 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 lactational 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, 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 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.

 

Remember also 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 five 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.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 below here) 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 when reading that about  PBDE effects in the EU, bear in mind that PBDE exposures in the U.S. have been found to be many times higher than in Europe.

 

For further evidence that widespread background exposures of infants to PBDEs (as received via breastfeeding, at least) are strong enough to have adverse effects on children, see Figure 5 and accompanying text at www.male-development.infoHowever, the adverse effects may only be seen at or closer to adulthood. (see Section 3.f)

 

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  Comparison with average adult exposure is also extreme:  As mentioned, a U.S. study estimated PBDE intake from food for nursing infants to be over 300 times higher than that for adult females.18d   

 

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 increases of body burdens of PBDEs since birth were over six times as high in 4-year-old children who had been breastfed as 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

 

………………………………………..

 

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

 

……………………………

 

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 increases of body burdens of PBDEs since birth were over six times as high in 4-year-old children who had been breastfed as 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) can be found at www.male-development.info

 

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 -- 0.7 TEQ/kg bw/day for dioxins) established by the EPA; this has been found in studies from many countries carried out during the 2000’s.73a The EPA's RfD is compatible with WHO's closest equivalent to the RfD, which states that "the upper range of the TDI (tolerable daily intake) of 4 pg TEQ/kg bw should be considered a maximal tolerable intake on a provisional basis and that the ultimate goal is to reduce human intake levels below 1 pg TEQ/kg bw/day."73b (emphasis added)  Dioxin has also 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 in early weeks after birth in the U.S. are in the upper part of the range (roughly 300 times the RfD) indicated above, but they taper 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; declines of birth rates 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 toxins 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.

 

Boys with higher dioxin exposure, but not girls with such exposure, were found to have decreased expressive communication scores.118g (Remember the 4.5-to-1 male-to-female ratio of autism, as well as impaired communication being a core trait of ASD.)  In another study, both boys and girls with higher exposures to a specific type of dioxin via breastfeeding had "significantly higher Autism Spectrum Rating Scale (ASRS) scores," and boys had significantly lower neurodevelopmental scores in relation to elevated total dioxin exposures via breastfeeding.118h

 

 

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 U.S. ATSDR shows compatible data indicating over-150-times-greater intake of mercury via food than via air.96a

 

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 indicated in the ATSDR data referred to above), 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 most of the accumulated mercury to an infant. 84,85 

 

For more studies finding associations between mercury levels and autism, see www.breastfeeding-and-lead.info.

 

 

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.

 

………………………..

 

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.

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.

 

Lead:  The following is a brief summation of information that is explained much more fully, with citations of authoritative sources, at www.breastfeeding-and-lead.info.

 

According to the EPA, 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  Lead is transferred to infants in breast milk, and it is transferred in doses high enough to significantly increase risk of neurodevelopmental harm.  Tests by the 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. (These results were low compared with what had been found in earlier decades, before use of lead solder in cans was discontinued.)

 

Blood lead levels below 2 µg/dL have been associated in many studies with neurological impairments. CDC data shows that over 3% of U.S. children in 2015 have blood lead levels much higher than that, indicating that many thousands of U.S. infants would have lead levels well into 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.  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.   

 

Associations have been found in many studies between autism and heavy metal (lead and mercury) exposure at levels often occurring in developed countries.  Many studies have also found associations closely linking ADHD with such lead exposures.

 

For much more complete information on this topic, including references to authoritative sources, see www.breastfeeding-and-lead.info.

 

Section 3.f:  Effects of these toxins becoming apparent in later childhood and adulthood, while often not being noticed earlier:

 

Considering the major, widespread presence of recognized developmental toxins in human milk (as presented earlier 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.  Also, various studies have been carried out that have found no harmful effects of the toxins as of early childhood, and on the basis of that the authors declare that the toxins in breast milk do not cause harm. 

 

There is, in fact, 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, discussed earlier:  PCBs, dioxins, mercury, lead, and pesticides; 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.  According to a team of researchers who are authors or coauthors of over 750 studies, when discussing "neurotoxic effects of perinatal exposure to PBDEs" as investigated in animal studies, "the main hallmark of PBDE neurotoxicity is a marked hyperactivity at adulthood.  Furthermore, a deficit in learning and memory processes has been found at adulthood in neonatally exposed animals."38p

 

Statements by authoritative agencies summarize what is known about lack of observable effects of these toxins during infancy, as well as about 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 U.S. infant formula in recent years.)

.  

Animal experiments provide confirmation of the human studies, regarding increased effects with age.  See Appendix I.

 

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's 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 to toxins that are undisputedly high in human milk, including effects that are often observed only after years or decades, one may wonder why a thinking person would bother to discuss what is apparent only during infancy.  

 

For more on the subject of long-term effects of breastfeeding, see Section 10

 

 

Section 3.g:  Each of the above toxins has been found to be present in typical human milk in concentrations exceeding the established safe level for that individual toxin (as summarized in this subsection), and their combined effects are likely to be more than merely additive.

 

According to the former chairman of the Canadian Institute of Child Health, the total effects of toxins such as those mentioned above are likely to be much more than merely the sum of their individual effects, actually being "more than multiplicative."  He referred to PCBs and dioxins as interacting especially synergistically.37e  An assessment by the ATSDR of interactions of toxins in breast milk, specifically, found two combinations to be synergistic, four to be additive, and two to be antagonistic.37f

 

 

 

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 receiving that much breastfeeding; that meant a 130% higher odds of having had that much breastfeeding, 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 section, studies will be presented that did not investigate breastfeeding directly 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 the autism-related outcomes.

 

Section 4.a.2.1:  Emissions from municipal incinerators were found to be closely associated with all of the autism-related outcomes that were investigated, but only in children who had been breastfed:

 

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, as indicated by parental concerns in specific developmental areas and at certain ages.  In breastfed children, adverse effects associated with the local incinerator on measured outcomes were reported in all four developmental areas that were asked about, at the latest age for which such results were reported. By contrast, among children in the general population who had similar exposure to the incinerator emissions, an adverse effect was found in only one area.  Also, much greater statistical significance was found of the effects on breastfed children compared with the significance of the one effect seen in children in the general population.119j

 

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

 

 

It is noteworthy that all of the above findings about adverse effects distinctly on breastfed children were almost hidden, in a back corner of the study, well past the main text.  This information was placed after the extended listing of footnotes, with no clues in the main text about other significant data being available to be seen somewhere else; when the breastfeeding-related data can finally be seen, 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 to be found within that paragraph.

 

It is safe to say that, if an exposure being studied were to be found to have far 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.  One can only wonder how many other findings about adverse effects of breastfeeding have gone unreported or have been essentially hidden from normal view.

 

Q:  Why are emissions from waste incinerators likely to be causes of ASD or other neurological impairment?   A:  They contain known neurodevelopmental toxins -- see Appendix K.

 

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

 

Section 4.a.2.2:

 

(a) Fairly common pesticide exposures have been closely linked with autism risk, in many studies (details below);  

 

(b) breast milk is the predominant pathway for pesticides to most infants, at a stage of high developmental vulnerability. (details below)

 

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

 

There have apparently been no studies that have investigated associations directly between autism and infants' ingestions of pesticides via breast milk; but logical combinations of studies enable us to see a real link between that exposure and that endpoint.  Later 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 relatively common, rather than 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  (remember from Section 2.a that the year after birth is a time of very high vulnerability of the developing brain to toxins);  correlation with exposure during the year after birth directly implicates exposure via breastfeeding, especially in communities with high breastfeeding rates such as in the above study; more on this will follow.

  

Evidence indicating that infant exposures to pesticides are predominantly via breastfeeding, including in an agricultural community:

 

The evidence on this topic is extensive.  A 2011 study that examined many different “exposure prediction factors” that could contribute to children’s levels of metabolites of organophosphorous pesticides in an agricultural community.139a  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. 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, even those living not far from agricultural fields, 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. 

 

For a much more complete presentation of the evidence indicating that breastfeeding is the predominant pathway for pesticides to infants, including the expert statement, 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...," and authoritative findings of absence of pesticides in infant formula, see Section B.3 in www.pesticides-and-breastfeeding.info

 

To summarize briefly:

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

  

(b) most pesticides are neurotoxic; fairly common background exposures to pesticides have been associated with autism in many studies; substantial lactational exposures to pesticides come during infants' vulnerable developmental periods;

 

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

 

Progression from (a) to (c) above, with breastfeeding leading to increased autism risk, appears to be very compatible with the evidence presented. Connecting a few dots here provides useful evidence on this topic, in addition to other evidence pointing in the same direction in Section 4.a.1.

    

For additional evidence of links between pesticide exposures and autism, see Appendix F.

For information about effects of pesticides in increasing the risk of ADHD, see Section B.2 of www.pesticides-and-breastfeeding.info.

 

 

 

Section 4.a.2.3:  Exposures to toxins in the first year after birth have been found to be strongly associated with risk of autism.  Toxins that are logically implicated are taken in by infants very predominantly via breastfeeding.

 

Notice in the chart below, from a review article,118a that odds of autism in association with high early-postnatal exposures to traffic-related air pollution were over three times as high as normal, dwarfing the equivalent odds for prenatal exposures. The research team (Volk et al., 2013) that found these outstandingly high odds for effects of early-postnatal exposures were authors or co-authors of over 850 published studies.

Fig. 6.0.d

image051.gif

Chart from Figure 2 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855851 

 

 

So the question obviously comes up as to which of the many different components of traffic-related emissions might be causing increased autism.  There has been considerable research and speculation on this question, but so far most of it seems to have been centered around major components of air pollution (NO2, SO2, etc.) that are not recognized developmental toxins. Research regarding autism in relation to those components that are not recognized developmental toxins has yielded minimal-to-moderate associations; such associations could be found merely because those components co-vary with atmospheric pollutants (from the same polluting sources) that are genuinely causal.

 

It would seem to be logical to look at least as much at pollution components that, although lower in volume, are known to be neurodevelopmental toxins.  A list of recognized developmental toxins, some of which are significant components of traffic-related air pollution, was provided in a 2016 scientific consensus statement; that statement (the TENDR statement) was signed by a group that includes 38 scientists and MD's, many of whom are highly-published authors of scientific studies.  It provides a list of six "prime examples of toxic chemicals that can contribute to learning, behavioral, or intellectual impairment, as well as specific neurodevelopmental disorders such as ADHD or autism spectrum disorder:"118j Of the six chemicals on that list, three are very significant components of traffic-related air pollution:  PCBs, PBDEs, and mercury. 

 

PCBs in traffic-related pollution:   In a 2013 U.S. study of PCB concentrations in carpet dust in homes at various distances from possible pollution sources, PCB concentrations were found to be about five times as high in homes within 600 yards from major roads in Los Angeles as they were in homes that were over 1100 yards from those roads;118c the p-value for this finding was <.01, indicating a high level of statistical significance.  As an indication of one specific potent source of PCBs in traffic emissions, PCBs have been found to be far higher in exhausts from older diesel engines, which are very commonly in use, than in emissions from newer engines.118d  Another near-traffic-versus-far-from-traffic difference in PCB exposure was found in a study in Colombia; measurements of PCBs (as well as dioxins) taken near vehicular sources were found to be almost six times as high as measurements made over a mile farther away.118e  

Selection from Figure 4

image060.gif 

In determining how likely an infant is to be significantly affected by PCBs from traffic emissions at its stage of high developmental vulnerability (early months after birth -- see Section 2.a), we need to consider the following matter:  There is considerable evidence about very different concentrations of PCBs taken in by infants according to type of feeding received (see Sections 2.b and 3.a.2 earlier, which include these charts).  Those contrasting intakes of developmental toxins, varying according to feeding type,  might well determine whether or not the infant's development is harmed by the traffic-related toxins.

 

PCBs' autism-related developmental toxicity:  Remember from Section 3.a the considerable evidence indicating, among other things, that PCBs "impact normal brain development" and "are associated with ... deficits in IQ, memory, language and school performance;” and lead to "chronic effects on a range of social and anxiety-related behaviors."

 

PBDEs in traffic-related pollution:  Although these chemicals are best known as flame retardants, they are also products of combustion, including traffic-related emissions.  Major presence of PBDES in traffic emissions is a probable explanation for why urban air has been found to have almost ten times the concentration of PBDEs as rural air, as reported by the U.S. ATSDR.118p  A Taiwanese study found that concentrations of PBDEs in vehicle exhausts were 18 to 148 times as high as concentrations of PCBs, in the different vehicles tested;45 when noting this apparent far greater exposure to PBDEs in traffic emissions compared with PCBs, we should remember (from above) that PCBs themselves have been found to be highly concentrated near major roadways.

 

Again, greatly amplified exposure to the traffic-related toxins due to breastfeeding:  One study (by researchers who are authors of a total of over 740 studies) calculated that 91% of a typical U.S. breastfed infant’s total exposure to PBDEs was from breast milk.56e  Assuming such a percentage, a maximum of 9% of an infant's PBDE exposure would normally come directly, compared with the other 91% being transferred via the medium of breastfeeding. That would imply that the effective exposure of the infant to PBDEs in the traffic-related pollution would be multiplied at least ten-fold as a result of the concentrating effect of lactation:  the mother takes in PBDES by way of exposures of a full-size body to pollutants, the toxins "accumulate in maternal adipose tissue,"139e and are mobilized and excreted to a small infant during nursing.  A 10-fold amplification of exposure due to  breastfeeding may sound like a surprisingly large effect, but it is fully compatible with data from another study;139f and it is on the low side of the concentrating effect of lactation in relation to both PBDEs and their chemical relatives, PCBs, that has been found in many other studies (see Section 2.b). 

Fig. 6.0.e

image053.gifThere are many different "congeners" of PBDEs; but, as this chart (from 45) suggests, BDE 209 has been found to be by far the predominant congener in vehicular pollution.  See in the next several paragraphs about the EPA-recognized developmental toxicity of this traffic-related pollutant that becomes part of breast milk.

 

PBDEs neurodevelopmentally toxic if exposure is postnatal:  Remember from "Adverse effects of PBDEs" in Section 3.b the considerable evidence on this topic, a small part of which is the EPA statement that “the most sensitive outcome of PBDE exposure is adverse neurobehavioral effects following exposure during the postnatal period."  And farther along in that section, note the findings that prenatal exposures to PBDEs had no significant adverse effects on children at age 4, but exposures via breastfeeding were associated with large increases in attention deficit problems and a 160% increased relative risk of poor social competence.57 (notice traits that are related to autism)  Also note the findings that lactational exposure to BDE 209, specifically, was associated with impaired cognitive development, and longer breastfeeding history was more strongly associated with neurodevelopmental impairment.58

 

To understand why prenatal exposures to certain chemicals should have no significant effects whereas postnatal exposures can have serious effects, note that (a) the placental barrier provides some protection to the fetus, (b) postnatal exposures are greatly amplified by the concentrating effect of breastfeeding, and (c) some sensitive stages of neurological development occur mainly or only during the months after birth.  See Sections 2.a, 2.b and 2.d for detailed discussion of these topics and references to authoritative sources.

 

 

In a 2014 document, the EPA rated 32 alternative flame retardants according to various characteristics, and BDE 209 was one of only three that received a "high" rating (the highest rating received) for developmental toxicity.56b Remember from preceding paragraphs that

-- a breastfed infant's exposure to PBDEs has been found to be overwhelmingly via breastfeeding,56e

 

-- the highly-developmentally-toxic BDE 209 has been found to be very strongly present in traffic-related emissions, and

 

-- neurological impairment has been found to be associated specifically with BDE 209 in human milk.

 

 

Substantial presence in human milk of developmentally-toxic, traffic-related PBDEs:

According to data from Health Canada (a department of the Canadian government), an infant would be expected to ingest about 800 to 9000 times as much BDE 209 via breast milk as via infant formula.56  This toxin's especially high presence in human milk is at least partly explained by the fact that it accumulates in the body, as has been verified in multiple studies.45b Differences between breast milk and infant formula in concentrations of PBDEs in general have been found to be less extreme but still major. (See Section 3.b)  

 

In what appears to be the only published data comparing PBDEs in gasoline emissions versus those in diesel emissions, "PBDE concentrations measured from the exhaust of UGFVs (unleaded gasoline-fueled vehicles) and DFVs (diesel-fueled vehicles) were 46.7 ng/Nm3, and 29.1 ng/Nm3, respectively;"45 that is, about 60% more PBDEs in gasoline emissions than in diesel emissions.  Therefore, when noticing how high BDE 209 has been found to be in diesel emissions (Figure 6.0.e), bear in mind that concentrations of this highly-developmentally-toxic chemical would very likely be even greater in mixed-traffic pollution, the type of pollution that was linked with especially high risk of autism. (Figure 6.0.d)

 

Remember (from above) that

 

-- PCB residues have been found to be many times more concentrated near major roads than farther away;

 

-- PBDEs have been found in vehicular emissions in far higher concentrations than PCBs;

  

-- the specific type of PBDE (209) that is apparently the one that is most concentrated in vehicle emissions is considered by the EPA to be high in developmental toxicity; PBDEs in general have neurodevelopmental toxicity linked with effects that are similar to traits of autism;

 

-- good evidence indicates that postnatal, not prenatal, exposures to these chemicals have the predominant toxic effects;

 

 -- an infant's exposures to PBDEs (and PCBs) from traffic-related pollution can become ten times higher as a result of breastfeeding.

 

 

Consider whether the combination of these factors could help explain the outstandingly high risk of autism that has been linked with traffic-related pollution specifically during the year after birth (as in the Volk et al study in Figure 6.0.d above). 

 

It would seem that a finding of such greatly increased risk of autism, reasonably connected with known exposures to recognized developmental toxins, should deserve close attention, especially since something can be easily done to drastically reduce the implicated exposures.  The infant feeding that concentrates and channels recognized developmental toxins to infants at a time of hazardous exposure could be replaced by the feeding type that was normal and apparently quite satisfactory for the generation that was born in the mid-20th century; that generation that did not have the many epidemics and increases of non-communicable disorders that have become prevalent since then. (see Section 13.b)

 

Hypotheses about effects of NO2, SO2, etc, in traffic-related pollution center around pollutants that are not recognized developmental toxins, and (perhaps not surprisingly) the risk ratios associated with those pollutants have been found to be comparatively minimal, at levels that are compatible with those substances' having no causal effect on autism risk.  In any case, greatly reducing most of those pollutants in vehicle emissions would be difficult or impossible.

.................................. 

 

There was one especially noteworthy observation to be made in the study that was the source of the earlier chart about traffic-related pollution exposures and odds of autism:  The odds of autism in relation to the pollution, as shown in Figure 2 of that study, were far lower for diesel pollution than for mixed-traffic pollution.118a  That brings to mind comparisons that have been made of the two main kinds of vehicular pollution with regard to their contents of mercury -- which is another one of the six "prime examples" of toxins that can affect development, as named in the TENDR statement.  A 2007 U.S. study, partly supported by the EPA, found that total mercury content in gasoline was 4.5 times the mercury content in diesel fuel.118m  Another 2007 study found mercury content of gasoline to be over three times as high as mercury content of diesel fuel.118n And remember from earlier that PBDE concentrations in gasoline emissions were found to be 60% higher than in diesel emissions.45

 

So the far higher levels of at least two recognized developmental toxins in gasoline than in diesel fuel (and/or in their emissions) may explain why adverse developmental effects of mixed traffic pollution have been found to be significantly higher than effects from diesel pollution.  That adds to the already substantial evidence (see Sections 3.d and 3.b) suggesting that exposures to those toxins lead to higher risk of autism.  Possibly more significantly, the facts that both of those toxins are present in human milk in many times higher concentrations than in infant formula (see above-linked sections) could mean that exposures of developing infants to harmful effects of traffic-related pollution could be sharply reduced by parents' no longer breastfeeding if they live near major roads.

 

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

 

Most studies have been assessing only prenatal exposures, in conformity with the widely-held notion that postnatal exposures do not have significant harmful effects on neurological development.  For many reasons as explained in Section 2, that belief is mistaken, and it contributes to failure to see the real causes of cognitive and other impairments.  The Volk et al. 2013 study, results of which are shown above (Figure 6.0.d), was and apparently still is one of a kind:  it is apparently the first and only study published as of November, 2016 in which effects were investigated of early-postnatal exposures to substantial mixed-traffic-related air pollution, as determined by measurements that reflected the complete mixture of traffic-related pollution.118b  The very high odds ratio for autism in relation to postnatal exposures to traffic-related pollution, as found in this study, is an illustration of the kind of thing that is typically missed when researchers neglect to measure postnatal exposures and effects.  In the search for solutions to serious health problems, an even worse turn away from a useful path occurs when funding sources waste money on research that fails to look at easily-examined, likely postnatal sources of harmful exposures.

 

 

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

 

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:

--  Of 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 study's 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 problematic sucking behaviors within two weeks after discharge from the hospital;119d unpleasant traits of autism could very well be emerging soon enough after birth to cause early weaning.

 

Another study (Burd et al., 1988, also showing ASD associated with early weaning) 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 (observational, according to the U.S. Surgeon General) that leading authorities on medical evidence consider to be of low quality (see Section 10); and

   b) over 50 studies (in addition to those cited earlier in this section) 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 a slowdown and then much slower growth.  Disabilities in American children followed that same general pattern, with especially large increases in disabilities among children born in the mid-80’s compared with children born in the early 1970’s (see Figure 11 and accompanying text); increases in later years were much slower.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

 

For most childhood diseases, historical health data for earlier decades is not sufficiently complete to show whether there was a minor decline that corresponded to the mild dip in breastfeeding during the 1980's; but data for childhood cancer does appear to be sufficient in that regard; see Figure 12.3 and accompanying text.

 

Note in the above chart that the overall breastfeeding rate increases in relation to the 1970 rates were especially dramatic in the case of longer-term breastfeeding.

 

Remember that

  (a) the above-discussed transfers of toxins 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; 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 each of the subsections of Section 3 above.)

 

 

 

 

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 following is a brief summation of a document that will be found at www.male-development.info when it is completed, which will probably be by Nov. 20, 2016. 

 

The very high ratios of males to females among children affected by the increasing neurological disorders (especially ASD and ADHD) have been basically unexplained.  Disproportionate problems among boys and young men have also reached well into the general population, in education and psychologically, far beyond those with diagnosed disorders.  Again, there is nothing but speculation as to the cause of this disparity.  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.  Looking back at when the boys would have been infants who would have been the first to widely have these problems as they grew older, one can see the mid-to-late 1970’s as the likely birth years of the boys and young men who would later have been the first ones having the problems of concern here.  Breastfeeding rates were very rapidly increasing during that period; human milk is clearly a major source of infant exposure to developmental toxins from the environment (see Section 3).  Apparently nobody knows about existence of any other major pathway for developmental toxins to infants in doses exceeding established safe levels. (see Section 6).

 

Typical exposures of human infants via breastfeeding to the toxins discussed here have been in doses far exceeding the relatively safe doses established by U.S. government agencies (in the cases of PCBs and mercury); or typical exposures of breastfed infants have at least been substantial (in the cases PBDEs, lead and many pesticides).  And authoritative testing has found little or none of those chemicals in contemporary infant formula in the U.S. (see Sections 3 and 8)

 

 

 

Section 8:  Pesticide effects and comparative exposures of infants: 

 

 

The following is a brief summation of information that will be found in more complete form, with references to authoritative sources, in a web document at www.pesticides-and-breastfeeding.info.

 

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. By highly-authoritative sources, human milk has been found to normally contain many pesticides, and infant formula in the U.S. has been found to contain essentially none. Exposures of children to pesticides at current background levels correlate well with reduced mental capacities as well as with ASD, ADHD, and other neurodevelopmental problems, in many studies

 

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. Two leading experts on toxins involved in child development have reported 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." A 2011 study found that the largest source of exposures to pesticides for most infants was breastfeeding, even in an agricultural community.

 

To read the much more complete form of the above, with references to authoritative sources, go to www.pesticides-and-breastfeeding.info.

 

 

 

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 at least 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 specific 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).  There are apparently no other toxins to which developing children are widely exposed that exceed established safe levels, aside from those four, as indicated by the responses to letters on this topic addressed to many organizations and scientists with appropriate expertise.  None of the several replies that were received suggested any.other toxins that might reach infants in doses recognized to be excessive. (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 and the Johnson-Restrepo et al. study in which it was calculated that 91% of a typical U.S. breastfed infant’s total exposure to PBDEs was from breast milk.56e  Similar extremes of exposure to PCBs would also come from breastfeeding, as indicated in Section 3.a

 

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

 

Section 9.b: In those early-postnatal months, other neurological development (in addition to that described in Section 2.d) is 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 of children 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;

(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).  The downward trends in development of children in those areas, paralleling the increases in exposures to those toxins, might not be coincidental.

 

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

 

………………………..

 

Section 10:  Poor evidence to support breastfeeding:  observational studies and outcomes assessed only in early childhood

 

Section 10.a:  Authoritatively recognized low quality of the kind of studies (observational) that have found benefits of breastfeeding

 

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 caused by the confounders.  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  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 

 

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 treatment 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 There are good reasons why the leading authorities on medical evidence have such low opinions of observational studies (see earlier in this section); such studies are thrown off by confounders such as the adherer effect.

 

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 a specific recommendation is useless.

 

image042.gif
 

Good adherence to recommendations --- even taking sugar pills — is associated with better health outcomes.

 

The above chart drew its data from "the placebo arms from eight studies."151  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 pills.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.  And the adhering mother would normally also be faithfully following the general and medical recommendations to breastfeed, so that better child health would be associated with breastfeeding even if the better health actually resulted entirely from the mother's general health-related behavior

 

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 confounder of socio-economic differences:  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 babies 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.

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

 

There is another lesson to be learned from the case of hormone replacement therapy, which Dr. Avorn (introduced above Figure 12.1) 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, before long-term effects could be observed.  The next section will deal with long-term effects of breastfeeding.

 

 

Section 11:  Promotion of breastfeeding is based mainly on observations of what appear to be short-term benefits; the evidence about longer-term effects strongly indicates worse long-term health outcomes. 

 

Remember from Section 3.f that long-term effects of toxins found in human milk have been detected well past early childhood, often only past early childhood.  Many studies were cited in that section, in which long-term effects of these toxins were found in areas related to IQ and other neurological functions, with the adverse effects sometimes found to increase with age.  EPA scientists referred to “long-latency delayed neurotoxicity” when discussing effects of toxins such as are contained in human milk; (those toxins are minimal or absent in infant formula -- see near beginnings of Sections 3.a to 3.e); similar statements about long-term effects of these toxins have been made by the U.S. ATSDR, WHO, and a commission of the U.S. National Academy of Sciences.  (Details and citations of sources for all of the above can be found in Section 3.f)

 

The U.S. Surgeon General's Call to Action to Support Breastfeeding 2011 makes 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), former Surgeon General Regina Benjamin went on to discuss associations of formula feeding with longer-term effects. (p. 2)  In that regard, her document asserts that "formula feeding is associated with higher risks for major chronic diseases and conditions... which have increased among U.S. children over time."  Given that, it certainly makes sense to consider the trends in recent decades in childhood diseases in relation to trends in infant feeding types; after all, there have been substantial changes in both in recent decades.  The Surgeon General's document does not go into any detail regarding changing levels of formula feeding in relation to increases of the diseases she specifies, so we will do so here:

 

 Fig. 12.2

image046.gifFirst, we need to remember the time trend of breastfeeding in the U.S., which began rapidly increasing in the early 1970's.  (See chart from the Surgeon General's document on left.)

 

Considering the first of the three diseases mentioned by the Surgeon General regarding increases over time (type 2 diabetes), note the following:

According to the president of the American Diabetes Association, type 2 diabetes as of 2002 had "changed from a disease of our grandparents and parents to a disease of our children."   At that time it was on its way to being what she called a "new epidemic" among children and young adults.152a  According to the only readily-found study on the history of the increase of childhood diabetes, "the rising incidence of the condition was not widely recognized until the 1980s;"152b and the first reference found by this author (after substantial search) to inclusion of young adults within this epidemic was in 2002.  All of this points toward a beginning of the major increase in childhood diabetes coming some time after the start of the rapid increase in breastfeeding.  (For much more information on this topic, see www.breastfeeding-and-diabetes.info.)

 

The next increasing disease to which Surgeon General Benjamin referred, when discussing presumed adverse effects of formula feeding, was asthma.  Newacheck and Halfon (2000) reported that the prevalence of disabilities related to asthma among U.S. children (based on the National Health Interview Survey) increased 232%, or more than tripled, during the period from 1969–1970 to 1994–1995.152c  Notice how similar that is to the increases in breastfeeding that took place during those years. (see Figure 12.2 just above)  By contrast, serious cases of asthma among adults were stable during the portion of that period (1980 and later) for which data is readily available.152d  (For more information on this topic, see www.breastfeeding-and-asthma.info.) 

 

Surgeon General Benjamin also referred to the increase in leukemia as relevant to consideration of the "risks" of formula feeding.  Since this discussion is about general health effects of breastfeeding versus formula, it would be much more meaningful here to discuss increases in childhood cancer in general.  But first, we should review Figure 12.2 not far above and especially note the following in that chart:

-- the very rapid increases in breastfeeding from 1972 to 1982,

-- the subsequent dip lasting for a decade or so,

-- the surpassing of the earlier peak about 16 years after the beginning of the dip, and then

-- increases continuing but at a slower rate than earlier, with minor fluctuation.

  Figure 12.3

(Chart excerpted from chart at image047.gifhttp://seer.cancer.gov/csr/1975_2013/results_single/sect_28_table.02.pdf )

.

In the data for childhood cancer in All Sites as shown in this chart, see how closely the pattern indicated by these figures resembles the pattern of breastfeeding increases. The trend for all cancer sites has the following characteristics:

 

-- substantial increases from 1975 to 1985 (or until later -- no data is provided by cancer.gov for 1986-1989),

-- followed by a minor dip for a decade or so,  

-- rising above the earlier peak 1-1/2 decades later, and

-- a mild increase in the final decade, with minor fluctuation.

 

It would not be unreasonable to consider the changes in childhood cancer incidence (described above) to be a somewhat-smoothed-out version of the changes in breastfeeding rates, with the turns in child cancer diagnoses lagging several years behind the turns in breastfeeding rates. 

 

It should not be surprising that average childhood cancer diagnoses would lag only three or four years behind related exposures, since:

   -- first childhood cancer diagnoses are at peak frequency at age 1, and they continue to be far more frequent at ages 2 through 4 than in the later years through age 14;152f 

   --  according to a publication of the National Academies Press, latencies of childhood cancers after exposures to carcinogens can be as little as a few months;152g latencies for childhood cancer are known to be especially short because of the rapid cellular proliferation taking place at that stage (see Figure 2); latencies even for some adult cancers have been determined to be only 4/10 of a year.152h

 

The similarities between the changing breastfeeding rates and changes in subsequent childhood cancer increases could be regarded as coincidental except for the fact that some of the toxins known to be present in breast milk (including dioxins), in concentrations greatly exceeding established safe levels (see Section 3), are considered by U.S. government agencies to be either known or suspected carcinogens; and there are many close correlations of high childhood cancer incidence with higher breastfeeding rates, by geographic location as well as by time period; for more information on this topic, see www.breastfeeding-and-cancer.info .

 

Remember that it was former Surgeon General Benjamin, a strong promoter of breastfeeding, who brought up the subject of increases that have been taking place in childhood diseases when she was discussing the alleged risks of formula feeding.  (She probably did so without having first looked closely at how the different trends actually compared.)  If the parallel trends (increasing exposures and increasing disease) are what might be expected on the basis of undisputed high levels of toxins contained in the exposure, they are a reasonable addition to the evidence to be considered.

 

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

 

There were other child disorders, increases of which the Surgeon General said we should consider in relation to changes in formula feeding.  Another one is obesity, which has more than tripled in recent decades, and which also deserves a close look in relation to breastfeeding trends.

Fig. 12.4

image050.gifNotice in this chart (using CDC data, again) that childhood obesity was relatively low for both of the age groups shown as long as the births of the specific age groups would have been before the time of rapid increases in breastfeeding.  But, by the time all children in an age group would have been born in the time of greatly increased breastfeeding, obesity of that age group had tripled or quadrupled.  And obesity percentages were at intermediate levels in the intervening years, during which only part of each age group would have been born during the time of greatly increased breastfeeding. And obesity has increased still further in more recent years,144 as breastfeeding has continued to increase.

 

 

Another long-term outcome, risk of which was considered by Surgeon General Benjamin to be increased by formula feeding, was Sudden Infant Death Syndrome.  As in the above cases, a close look at the historical data for both SIDS incidence and formula feeding shows nothing by way of compatible trends; also, a close look at the quality of the studies on this topic, as assessed by authoritative sources, reveals that most of the studies considered by reviewers to be of high quality show no correlation between SIDS and formula feeding.  See www.breastfeeding-and-SIDS.info

 

Aside from what is revealed by the historical record, 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)  A high percentage of those studies have made their assessments well past early childhood.

 

 

Section 12Randomized trials, although still subject to bias, are recognized as being superior to observational studies, and they provide far better evidence about effects of breastfeeding.

 

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.  (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:

 

A 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.  Developmental quotient scores (at nine months) of infants fed partially with formula were higher than those of 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 from another randomized trial, one that shows results that are in sharp conflict with the usual observational studies that have found benefits of breastfeeding.

 

 

Figure 12.5

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.

 

Still another way of avoiding the weaknesses of observational studies is sibling studies, as a way of trying to make sure that comparisons are valid; a 2014 sibling study found that asthma was “one outcome for which breastfeeding duration is consistently associated with poorer childhood health and wellbeing across all three models.”152e

 

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 Section 13 just below). 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 and highs and lows of breastfeeding rates geographically and according to time -- see www.breastfeeding-and-diabetes.info. 

 

 

Section 13:  Final remarks

 (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.)

 

Section 13.a:   A reasonable question to consider:

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

 

Section 13.b:  A viable alternative to breastfeeding:

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 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 the environment (and therefore in human milk) had already begun in the 1940's and 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: 

 

Trend of chronic childhood health conditions since the 1960's, while breastfeeding was increasing:  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.

 

…………………………

 

  

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. Remember from the discussion of "observational studies" (in Section 10) 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.

 

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

The American Academy of Pediatrics, despite the very ample evidence of developmental toxins in average human milk (see 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, as stated above, was overwhelmingly normal for the generation born in the mid-20th-century U.S.,134 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 breastfeeding was rare, considering the levels of developmental toxins in recognized excessive doses in human milk, as opposed to in the main alternative. (see Section 3)

 

 

Comments or questions on the above are invited, including criticisms if they are specific, and will usually receive a response.  At the next link are past comments and questions from a number of readers, including eight doctors, followed by our responses.  Some of the doctors have been critical but others have been substantially in agreement with us (including one with children with asthma, one who says she has delivered thousands of babies, and one with a son with autism); they put into briefer, everyday language and personal terms some important points that tend to be immersed in detail when presented in our own publications.  Topics discussed in that section include about having breast milk tested for toxins and about means of trying to achieve milk that is relatively free of toxins, including the “pump and dump” option.  To read the above, go to 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 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 in infant exposures.

 

A U.S. 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 possibly engaging in hand-to-mouth activity.

 

  

Appendix I:  Animal studies providing additional evidence of long-term/delayed effects of developmental toxins:

When reading this section, remember that, according to a consensus statement signed by an impressive list of 57 scientists, researchers and health professionals, "The concordance between human and animal neurotoxicity assessment is remarkable as demonstrated for lead, mercury and PCBs."36a

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.) is described in www.male-development.info  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 from that same website that testosterone is important to male mental functioning.Also see the Colciago et al. study in that same website about the strong effect on learning ability in adult rats that has been found to result from developmental PCB exposure, in an animal experiment.

  

Appendix K:  Emissions from incinerators that could be causes of autism and other neurological disorders:

 

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.  And dioxins are known typical contents of incinerator emissions, created as part of combustion processes that include burning of plastics.  All five of those chemicals have been found in potentially hazardous concentrations in typical 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.  For explanation of the concentrating effect of lactation, see Section 2.b.

 

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

 

 

 

 

 

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/

 

6a) GW Chance, Environmental contaminants and children’s health: Cause for concern, time for action,  Paediatr Child Health  2001 Dec; 6(10): 731–743. at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805986/

 

6b) 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/

 

6c) Colburn et al., Developmental Effects of Endocrine-Disrupting Chemicals in Wildlife and Humans, Environ Health Perspect., 1993, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1519860/pdf/envhper00375-0020.pdf 

 

6d) from Chemical & Engineering News, January 12, 1998, Copyright © 1998 by the American Chemical Society, at  http://pubs.acs.org/cen/hotarticles/cenear/980112/prodshipgraphs.html

 

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  "As observed in other studies, nursing infants consume a daily TEQ intake that is 50 times higher than adults."

 

(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

 

(18d) 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 October; 114(10): 1515–1520. Published online 2006 July 13. doi: 10.1289/ehp.9121PMCID: PMC1626425   at https://www.ncbi.nlm.nih.gov/pubmed/17035135

 

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/ 

-- Also, according to Encyclopedia Britannica, use of insecticides was considered to be responsible for a dramatic increase in agricultural productivity between 1945 and 1965. (https://www.britannica.com/technology/insecticide)

 

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

 

24b) American Academy of Pediatrics:  Pediatric Environmental Health, 3rd Edition, 2012, p. 200.

 

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

 

36a) Collaborative on Health and the Environment’s Learning and Developmental Disabilities InitiativeScientific Consensus Statement on Environmental Agents Associated with Neurodevelopmental Disorders, 2008, at http://ww.healthychildrenproject.org/pdfs/080801_Scientific-Concensus-Statement-LDDI.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

 

37e)  GW Chance, Environmental contaminants and children’s health: Cause for concern, time for action, Paediatr Child Health <#>. 2001 Dec; 6(10): 731–743. at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805986/

 

37f)  State of Washington Department of Ecology, Multiyear PBT Chemical Action Plan Schedule, at https://fortress.wa.gov/ecy/publications/documents/0707016.pdf, p. 62

 

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

 

38p) Branchi et al., Polybrominated diphenyl ethers: neurobehavioral effects following developmental exposure, Neurotoxicology. 2003 Jun;24(3):449-62.  at https://www.ncbi.nlm.nih.gov/pubmed/12782110 

 

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) Re presence of PBDEs in vehicular emissions, citing two other studies as well as its own findings about PBDEs in vehicular emissions, see 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, at http://aaqr.org/VOL11_No6_November2011/8_AAQR-11-05-OA-0058_709-715.pdf ;

    also from that study, "The GM PBDE concentrations measured from the exhaust of UGFVs (unleaded gasoline-fueled vehicles) and DFVs (diesel-fueled vehicles) were 46.7 ng/Nm3, and 29.1 ng/Nm3, respectively (Wang et al., 2010b), and the highly brominated PBDEs in urban ambient air were contributed by combustion sources, such as vehicles (Wang et al., 2010b, 2011)."

 

45a) Lorber M, Exposure of Americans to polybrominated diphenyl ethers, J Expo Sci Environ Epidemiol. 2008 Jan;18(1):2-19. Epub 2007 Apr 11. at https://www.ncbi.nlm.nih.gov/pubmed/17426733

 

45b) Frederiksen et al., Human internal and external exposure to PBDEs--a review of levels and sources. Int J Hyg Environ Health. 2009 Mar; at https://www.ncbi.nlm.nih.gov/pubmed/18554980

 

45c) Chuang et al., PCDD/F emissions from gasoline and diesel fueled vehicles, Sustain. Environ. Res., 21(1), 29-36 (2011) at https://www.researchgate.net/profile/Lin-Chi_Wang/publication/258332540_PCDDF_EMISSIONS_FROM_GASOLINE_AND_DIESEL_FUELED_VEHICLES/links/0c96052a944b19c2f6000000.pdf

 

Also Sakai et al., Section VI.H.:  Guidance by source category: Annex C, Part III Source Categories:  Motor vehicles, particularly those burning leaded gasoline

 

45d) Wang et al., Supporting information for Emission estimation and congener-specific characterization of polybrominated diphenyl ethers from various stationary and mobile sources, at http://120.118.219.14/bitstream/987654321/2051/1/EP2010-2%20SI.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.) at https://www.ncbi.nlm.nih.gov/pubmed/17711201

 

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  Note that, although decaBDE can consist of more than just BDE 209, the two are in practice so similar that the two designations are often used interchangeably. (Costa et al., Is decabromodiphenyl ether (BDE-209) a developmental neurotoxicant?  Neurotoxicology. 2011 Jan)

 

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

 

56b) EPA:  An Alternatives Assessment for the Flame Retardant Decabromodiphenyl Ether (DecaBDE), 2014. at http://www.epa.gov/sites/production/files/2014-05/documents/decabde_final.pdf

 

56c) 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

 

56d) Tozuka et al., Transfer of Polycyclic Aromatic Hydrocarbons to Fetuses and Breast Milk of Rats Exposed to Diesel Exhaust, Journal of Health Science 50(5) 2004, at http://jhs.pharm.or.jp/data/50(5)/50_497.pdf     pp. 497-502

 

56e) Johnson-Restrepo et al., An assessment of sources and pathways of human exposure to polybrominated diphenyl ethers in the United States, Chemosphere, 2009 Jul;76(4):542-8. doi: 10.1016/j.chemosphere.2009.02.068. Epub 2009 Apr 5.  at http://www.ncbi.nlm.nih.gov/pubmed/19349061 

 

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:  At Section 1.a.1, p. 2 of EPA IRIS Chemical Reference Summary document on dioxins at https://cfpub.epa.gov/ncea/iris/iris_documents/documents/subst/1024_summary.pdf:  RfD is shown as 7 × 10−10 mg/kg-day RfD (that is, 0.7 pg of TEQ/kg-d)    

 

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

 

- 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.

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

 

-  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

 

73b)  WHO Consultation, 1998:  Assessment of the health risk of dioxins: re-evaluation of the Tolerable Daily Intake (TDI) WHO Consultation (Executive Summary), p. 27, at http://www.who.int/ipcs/publications/en/exe-sum-final.pdf?ua=1

 

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), 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   Reported also in U.S. ATSDR, Toxicological Profile for Chlorinated Dibenzo-P-Dioxins, at http://www.seagrant.umn.edu/water/report/chemicalsofconcern/dioxins/dioxins.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

-- Also see Magos, The absorption,distribution and excretion of methylmercury.  In: The Toxicity of Methylmercury (Eccles CV, Annau Z, Eds) Baltimore: Johns Hopkins University Press, 1987; 24-44.

 

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

another study also found evidence of excretion of mercury during breastfeeding. (Vahter, Longitudinal Study of Methylmercury and Inorganic Mercury in Blood and Urine of Pregnant and Lactating Women, as Well as in Umbilical Cord Blood, Environmental Research, Volume 84, Issue 2, October 2000, Pages 186–194

 

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

 

93d) U.S. ATSDR:  Toxicological Profile For Chlorinated Dibenzo-P-Dioxins, p. 203, at http://www.seagrant.umn.edu/water/report/chemicalsofconcern/dioxins/dioxins.pdf

93e) NIH web page at http://www.nlm.nih.gov/medlineplus/ency/article/001193.htm  Also see EPA statement at U.S. EPA:  Toxicological Review of 2,2',4,4'-Tetrabromodiphenyl Ether (BDE-47) EPA/635/R-07/005F  www.epa.gov/iris, p. 40 at  http://www.epa.gov/iris/toxreviews/1010tr.pdf 

 

93f) A seven-scientist team of French researchers stated in a 2010 study that “TH (thyroid hormone) plays an important role in cerebellar neurogenesis, a mainly postnatal developmental process… perinatal hypothyroidism (leads to) a striking reduction in the growth and branching” of connections in the developing brain. (Boukhtouche et al., Induction of early Purkinje cell dendritic differentiation by thyroid hormone requires RORα, Neural Development 2010, 5:18  doi:10.1186/1749-8104-5-18  at http://www.neuraldevelopment.com/content/5/1/18)   In a 2000 article in the journal Cerebral Cortex, an Oxford Journal, it is stated that “neonatal TH deficiency severely impacts development…. Mental retardation resulting from neonatal thyroid hormone deficiency is an example….” (italics added) (Thompson et al., Thyroid Hormone Action in Neural Development, Cereb. Cortex (2000) 10 (10): 939-945. doi: 10.1093/cercor/10.10.939 at http://cercor.oxfordjournals.org/content/10/10/939.long)

 

 

93g)  Koopman-Esseboom et al., Effects of dioxins and polychlorinated biphenyls on thyroid hormone status of pregnant women and their infants, Pediatr Res. 1994 Oct;36(4):468-73. at http://www.ncbi.nlm.nih.gov/pubmed/7816522

 

Turyk et al., Relationships of Thyroid Hormones with Polychlorinated Biphenyls, Dioxins, Furans, and DDE in Adults, Published online May 31, 2007. doi:  10.1289/ehp.10179  at www.ncbi.nlm.nih.gov/pmc/articles/PMC1940071/

 

93h) U.S. ATSDR:  Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000 at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf, pp. 21, 18  The ATSDR refers to “extensively corroborated findings in experimental animals that exposure to PCBs in utero and/or during early development (e.g., through breast milk) can deplete levels of circulating thyroid hormones in the fetus or neonate, which may give rise to a hypothyroid state during development.”  The Danish Health and Medicines Authority says essentially the same thing except that they indicate greater certainty about the expected result of low thyroid. (Danish Health and Medicines Authority, 2013, Health risks of PCB in the indoor climate in Denmark, at http://sundhedsstyrelsen.dk/publ/Publ2013/12dec/HAofPCBindoorDK_en.pdf)

 

93j) Developmental Neurotoxicity of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Costa et al., Neurotoxicology. 2007 November; 28(6): 1047–1067.  doi:  10.1016/j.neuro.2007.08.007 PMCID: PMC2118052   NIHMSID: NIHMS34875 at  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052/

See also   U.S. ATSDR, Polybrominated Biphenyls (PBBs) & Polybrominated Diphenyl Ethers (PBDEs),  Section 4, p. 41 at http://www.atsdr.cdc.gov/ToxProfiles/tp.asp?id=529&tid=94

 

 

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

 

96a) Table 5-12, p. 532 of U.S. ATSDR:  Toxicological Profile for Mercury, 1999, Ch. 5, Potentialfor Human Exposure, at  http://www.atsdr.cdc.gov/toxprofiles/tp46.pdf   This table shows total daily intake of mercury in adults to be 0.04 micrograms per day via air exposure, compared with 6.6 micrograms per day via food.

 

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/

 

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.

 

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

 

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

 

105a) Tran et al., Impacts of Perinatal Dioxin Exposure on Motor Coordination and Higher Cognitive Development in Vietnamese Preschool Children: A Five-Year Follow-Up, PLoS One. 2016; 11(1): e0147655. Published online 2016 Jan 29, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4732982/

                                                                            

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   An image of part of the article is shown below, since it may be expensive for many readers to see the complete study.

Shambergerquote.gif

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

 

118a)  Kalkbrenner et al., Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence, Curr Probl Pediatr Adolesc Health Care, Author manuscript; available

in PMC 2016 May 4, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855851/

 

118b)  Other studies have been published that are not considered to be relevant here, since they did not take into account major known hazardous components of traffic-related emissions, including PCBs and dioxins;  they assessed only developmental effects of specified other components of traffic pollution. The Volk et al. study, going by distance from the freeways, would have encompassed all components of the vehicular emissions. 

   It has been suggested that particulate-matter pollution (PM) is relevant to traffic-related pollution, but it actually has only minimal relation to traffic-related pollution.  The EPA points out that PM is an indirect result of complex reactions of chemicals from various sources, with automobiles being mentioned as indirect sources only after emissions from power plants and industries; direct emissions of PM from various (non-traffic) sources are also mentioned.  So traffic-related PM could well be15% or less of all PM in air, and only indirectly resulting from traffic at that. 

 

118c)  DellaValle et al., Environmental determinants of polychlorinated biphenyl concentrations in residential carpet dust, Environ Sci Technol. 2013 Sep 17; 47(18): 10405–10414. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076890

 

118d) Laroo et al., Emissions of PCDD/Fs, PCBs, and PAHs from legacy on-road heavy-duty diesel engines, Chemosphere, 2012 Nov at https://www.ncbi.nlm.nih.gov/pubmed/22682896

  Also Hsieh et al., Reduction of Toxic Pollutants Emitted from Heavy-duty Diesel Vehicles by Deploying Diesel Particulate Filters, Aerosol and Air Quality Research, 2011, at http://aaqr.org/VOL11_No6_November2011/8_AAQR-11-05-OA-0058_709-715.pdf

 

118e) Cortés et al., PCDD/PCDF and dl-PCB in the ambient air of a tropical Andean city:  passive and active sampling measurements near industrial and vehicular pollution sources, Sci Total Environ. <#> 2014 Sep 1 at https://www.ncbi.nlm.nih.gov/pubmed/24555963  Note that PCDD/F is a designation for what is more commonly referred to as dioxins.

 

118f) U.S. EPA:  Update to An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000 (2013, External Review Draft), Table 1-12 , at cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=235432

 

118g) Tai et al., Effects of Perinatal Dioxin Exposure on Development of Children during the First 3 Years of Life, J Pediatr., 2016 Aug; at https://www.ncbi.nlm.nih.gov/pubmed/27189679

 

118h) Nishijo et al.,  2,3,7,8-Tetrachlorodibenzo-p-dioxin in breast milk increases autistic traits of 3-year-old children in Vietnam. Mol Psychiatry. 2014 Nov; at https://www.ncbi.nlm.nih.gov/pubmed/24637425

 

118j) Project TENDR: Targeting Environmental Neuro-Developmental Risks The TENDR Consensus Statement, Environ Health Perspect. 2016 Jul; 124(7): A118–A122. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4937840/

118k)  Wang et al., Emission estimation and congener-specific characterization of polybrominated diphenyl ethers from various stationary and mobile sources, Environ Pollut. <#> 2010 Oct; at https://www.ncbi.nlm.nih.gov/pubmed/20656384

 

118m) Landis et al., Ft. McHenry tunnel study: Source profiles and mercury emissions from diesel and gasoline powered vehicles, Atmospheric Environment, 2007, Volume 41, Issue 38 at http://www.sciencedirect.com/science/article/pii/S1352231007006607

 

118n) Won et al.,  Mercury emissions from automobiles using gasoline, diesel, and LPG, Atmospheric Environment,Volume 41, Issue 35  November 2007, Pages 7547–7552 at http://www.sciencedirect.com/science/article/pii/S1352231007004992

 

118p) Section 4.1 of ATDSR document on PBDEs at http://www.atsdr.cdc.gov/toxprofiles/tp68-c4.pdf

 

118r) Lorber M, Exposure of Americans to polybrominated diphenyl ethers, J Expo Sci Environ Epidemiol. 2008 Jan;18(1):2-19. Epub 2007 Apr 11. at https://www.ncbi.nlm.nih.gov/pubmed/17426733

 

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)   This study found a 37% rate of breastfeeding at six months among children diagnosed with autism, as compared with 13% in the control group. 

 

119a) Symptoms web page of Autism Speaks, at https://www.autismspeaks.org/what-autism/symptoms

Also Counseling blog of Autism Speaks, at https://www.autismspeaks.org/blog/2014/08/29/autism-anxiety-parents-seek-help-extreme-reaction-loud-noise

Also, doing a web search for “restless agitation autism” brings up many blogs from parents who use those terms to describe their children with autism.

 

119b) Odom et al., Reasons for Earlier Than Desired Cessation of Breastfeeding, Pediatrics. 2013 Mar; 131(3): e726–e732. PMCID: PMC4861949

 

119c) Children with autism at significant risk for feeding problems and nutritional deficits, Woodruff Health Sciences Center | Feb. 4, 2013  at http://www.news.emory.edu/stories/2013/02/autism_nutritional_deficits/

 

119d) Lucas et al., Dysregulated Breastfeeding Behaviors in Children Later Diagnosed With Autism, J Perinat Educ. 2015; 24(3): 171–180  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720870/

 

119e) Fung LK, Mahajan R, Nozzolillo A, Bernal P, Krasner A, Jo B, Coury D, Whitaker A, Veenstra-Vanderweele J, Hardan AY. Pharmacologic Treatment of Severe Irritability and Problem Behaviors in Autism: A Systematic Review and Meta-analysis.  Pediatrics. 2016 Feb;137 Suppl 2:S124-35.

-- McGuire K, Fung LK, Hagopian L, Vasa RA, Mahajan R, Bernal P, Silberman AE, Wolfe A, Coury DL, Hardan AY, Veenstra-VanderWeele J, Whitaker AH. Irritability and Problem Behavior in Autism Spectrum Disorder: A Practice Pathway for Pediatric Primary Care.   • Pediatrics. 2016 Feb;137 Suppl 2:S136-48. doi: 10.1542/peds.2015-2851L. Epub 2016 Feb 1..

--  Sukhodolsky DG, Smith SD, McCauley SA, Ibrahim K, Piasecka JB. Behavioral Interventions for Anger, Irritability, and Aggression in Children and Adolescents.  J Child Adolesc Psychopharmacol. 2016 Feb;26(1):58-64.

 

119f) Jones et al., Attention to eyes is present but in decline in 2-6-month-old infants later diagnosed with autism: Nature:(2013) DOI:doi:10.1038/nature  at www.pediatrics.emory.edu/documents/divisions/autism/Jones_Klin_2013.pdf

 

119g)  Lung et al., Incinerator Pollution and Child Development in the Taiwan Birth Cohort Study,  Int. J. Environ. Res. Public Health 2013, at www.mdpi.com/1660-4601/10/6/2241/pdf

 

119h)  See list of symptoms of ASD at http://www.autismkey.com/autism-symptoms/

 

119j) The adverse associations in breastfed children were found with p values of 0.003, 0.011, and 0.001 (four at 0.001); five of those six were much lower (less likely to result from chance) than the p value of .008 for the one area in which there was significant effect of local incineration on children in the general population.

 

120) Durkin et al., Advanced Parental Age and the Risk of Autism Spectrum Disorder, Am J Epidemiol. 2008 December 1; 168(11)  Table 3’s “Birth order” section, at  www.ncbi.nlm.nih.gov/pmc/articles/PMC2638544; this study was referred to in 2009 as the largest of its kind  (in “US researchers find link between age, birth order and autism,” theguardian.com, 7 January 2009).  Durkin et al. also referred to another study supporting correlation of increased autism with earlier birth order: Glasson et al. Perinatal factors and the development of autism. Arch Gen Psychiatry. 2004;61(6):618–627

 

121) Croen et al., Maternal and Paternal Age and Risk of Autism Spectrum Disorders, JAMA Pediatrics, April 2007, Vol 161, No. 4  http://archpedi.jamanetwork.com/article.aspx?articleid=570033#poa60107t3

 

122) Leonard et al., Autism and Intellectual Disability Are Differentially Related to Sociodemographic Background at Birth,  PLoS One. 2011; 6(3): e17875. Published online Mar 30, 2011  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068153 finding that “When compared with those who were first born, the odds for ASD with and without ID were reduced for those second or later born. In contrast the odds for children with mild-moderate and severe ID were increased for later born children.”

 

123) CDC chart at www.cdc.gov/breastfeeding/data/NIS_data/2006/socio-demographic.htm

 

124) Yang et al.,  PCDDs, PCDFs, and PCBs concentrations in breast milk from two areas in Korea: body burden of mothers and implications for feeding infants, Chemosphere 46 (2002) 419–428

 

125) see at http://www.doh.gov.uk/public/infantfeedingreport.htm, p. 8

 

126) Factors Influencing Full Breastfeeding in a Southwestern Ontario Community: Assessments at 1 Week and at 6 Months Postpartum  Tammy J. Clifford, PhD  Human Lactation, 2012

 

127) Lakind et al., Infant Exposure to Chemicals in Breast Milk in the United States: What We Need to Learn From a Breast Milk Monitoring Program  Judy S. LaKind, et al.,  Children's Health Review Environmental Health Perspectives • Vol. 109 | No. 1 | January 2001  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1242055/pdf/ehp0109-000075.pdf ; also  Infant Exposure to Dioxin-like Compounds in Breast Milk  Lorber1 and Phillips2  Volume 110 | Number 6 | June 2002 • Environmental Health Perspectives  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240886/

 

127a)  Duarte-Davidson et al., Polychorinated biphenyls (PCBs) in the U.K. population:  estimated intake, exposure, and body burden, Science of the Total Environment, Vol. 151, July 1994, at http://www.sciencedirect.com/science/article/pii/0048969794901708

128) Furst et al., PCDD and PCDF levels in human milk — dependence on the period of lactation. Chemosphere 18(1):439– 444 (1989). Referred to in Lakind et al., above

 

129)  Polder et al., Levels of chlorinated pesticides and polychlorinated biphenyls in Norwegian breast milk (2002–2006), and factors that may predict the level of contamination, Science of The Total Environment, Volume 407, Issue 16, 1 August 2009, Pages 4584–4590  at http://www.sciencedirect.com/science/article/pii/S0048969709003726  Parity was associated with decreasing organochlorine levels (P < 0.001)

 

130) Bajanowski et al., Dioxin in infants--an environmental hazard? Int J Legal Med., 2002 Feb;116(1):27-32, at http://www.ncbi.nlm.nih.gov/pubmed/11924704

 

131) R.C. Gupta, Ed., Reproductive and Developmental Toxicology, Burlington : Elsevier Science, 2011, ISBN: 978-0-12-382032-7, at http://www.sciencedirect.com/science/book/9780123820327. (pp. 551 and 559, Ch. 41, in Section 8)

 

132) Geraghty et al., Reporting Individual Test Results of Environmental Chemicals in Breastmilk: Potential for Premature Weaning, Breastfeeding Medicine. December 2008, 3(4): 207-213. doi:10.1089/bfm.2008.0120. at http://www.ncbi.nlm.nih.gov/pubmed/19086823

 

133) Gates v. Jensen, 92 Wn.2d 246 (1979), 595 P.2d 919, item (1), at https://casetext.com/case/gates-v-jensen-1.  The Court referred to two earlier cases in support of its “application of the doctrine of informed consent to circumstances other than treatment of a diagnosed disease.”

 

133a) Jandre and Jandre v. Wisconsin Injured Patients and Families Compensation Fund, 2012 WI 39, Supreme Court of Wisconsin, Case No.: 2008AP1972 , in par. 25, at   http://www.wicourts.gov/sc/opinion/DisplayDocument.pdf?content=pdf&seqNo=81164)

 

133b) Spatz et al., The New Era of Informed Consent:  Getting to a Reasonable-Patient Standard Through Shared Decision Making, Journal of the American Medical Assn., Viewpoint | May 17, 2016, at http://jama.jamanetwork.com/article.aspx?articleID=2516469

 

134) AAFP:  Breastfeeding, Family Physicians Supporting (Position Paper) -- at http://www.aafp.org/about/policies/all/breastfeeding-support.html

 

134a) Riordan et al., Basics of breastfeeding. Part I: Infant feeding patterns past and present, JOGN Nurs., 1980 Jul-Aug;9(4):207-10, at http://www.ncbi.nlm.nih.gov/pubmed/7001126

Other sources report the low point of breastfeeding to be 1971, based on breastfeeding “ever” or “at any time,” as opposed to the more extended breastfeeding that is more significant regarding health effects.

 

135) Jandre and Jandre v. Wisconsin Injured Patients and Families Compensation Fund, 2012 WI 39, Supreme Court of Wisconsin, Case No.: 2008AP1972 , in par. 25, at   http://www.wicourts.gov/sc/opinion/DisplayDocument.pdf?content=pdf&seqNo=81164)

 

136)  EM Roberts et al., Maternal residence near agricultural pesticide applications and autism spectrum disorders among children in the California Central Valley, Environ Health Perspect. 2007 Oct;115(10):1482-9, at http://www.ncbi.nlm.nih.gov/pubmed/17938740/  “comparing children of mothers living within 500 m of field sites with the highest nonzero quartile of organochlorine poundage to those with mothers not living near field sites suggested an odds ratio for ASD of 6.1 (95% confidence interval, 2.4-15.3)”

 

137) Roberts and English, Bayesian modeling of time-dependent vulnerability to environmental hazards:  an example using autism and pesticide data, Statistics in Medicine, Published online 7 September 2012 in Wiley Online Library (wileyonlinelibrary.com) DOI: 10.1002/sim.5600) at http://www.ncbi.nlm.nih.gov/pubmed/22961924

 

137a) See Section 4.a of www.autism-studies.net for several authoritative sources for this.

 

137b) Boumann et al., Malaria Control Insecticide Residues in Breast Milk: The Need to Consider Infant Health Risks, Environmental Health Perspectives, Vol. 117, No. 10, Oct. 2009, at http://ehp.niehs.nih.gov/0900605/

 

137c) see Section 4.a of www.autism-studies.info.

 

137d)  Kalkbrenner et al., Environmental Chemical Exposures and Autism Spectrum Disorders:  A Review of the Epidemiological Evidence, Curr Probl Pediatr Adolesc Health Care. 2014 Nov; 44(10): 277–318.  PMCID: PMC4855851 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855851

 

137e) Bouchard et al., Attention Deficit/Hyperactivity Disorder and Urinary Metabolites of Organophosphate Pesticides In U.S. Children 8–15 Years, Pediatrics. 2010 Jun; 125(6): e1270–e1277.  Published online 2010 May 17.  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3706632/

 

138) Bellinger, A Strategy for Comparing the Contributions of Environmental Chemicals and Other Risk Factors to Neurodevelopment of Children, Environ Health Perspect. 2012 Apr; 120(4): 501–507. PMCID: PMC3339460  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3339460/

 

138a) Shelton et al., Neurodevelopmental disorders and prenatal residential proximity to agricultural pesticides: the CHARGE study, Environ Health Perspect.,  2014 Oct;122(10):1103-9. doi: 10.1289/ehp.1307044. Epub 2014 Jan 23. at http://www.ncbi.nlm.nih.gov/pubmed/24954055

 

138b) 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/

 

139) Rossignol et al., Environmental toxicants and autism spectrum disorders: a systematic review, Transl Psychiatry. 2014 Feb; 4(2): e360. PMCID: PMC3944636  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3944636/  

 

139a). Bradman et al.,  Determinants of Organophosphorus Pesticide Urinary Metabolite Levels in Young Children Living in an Agricultural Community, International Journal of Environmental Research and Public Health ISSN 1660-4601, Table S-4, at http://www.mdpi.com/1660-4601/8/4/1061

 

139e) Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. Lancet. 2006;368:2167–2178. at http://www.reach-compliance.eu/english/documents/studies/neurotoxity/PGrandjean-PjLandrigan.pdf  p. 2 

 

139f) Gyalpo et al., Insights into PBDE Uptake, Body Burden, and Elimination Gained from  Australian Age–Concentration Trends Observed Shortly after Peak Exposure, Environ Health Perspect 2015 Oct; 123(10): 978–984.at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4590757/

 

140) Damgard and eight others, Persistent Pesticides in Human Breast Milk and Cryptorchidism, Environ Health Perspect. 2006 Jul; 114(7): 1133–1138. Table 2, at  www.ncbi.nlm.nih.gov/pmc/articles/PMC1513324/

 

141)  Weldon et al., A pilot study of pesticides and PCBs in the breast milk of women residing in urban and agricultural communities of California, Journal of Environmental Monitoring, DOI: 10.1039/c1em10469a, at http://ehsdiv.sph.berkeley.edu/holland/publications/files/Weldon2011.pdf  Also, Non-persistent Pesticides Found in U.S. Mothers' Breast Milk, Bridges, Spring 2012,  Regents of the University of California, Center for Occupational and Environmental Health, at http://coeh.berkeley.edu/bridges/Spring2012/PesticidesBM.html

 

144) Perrin et al., The Increase of Childhood Chronic Conditions in the United States, JAMA, June 27, 2007—Vol 297, No. 24,  2755 at http://www.childrensdayton.org/cms/resource_library/files/a6b01f3b8f8d5ebd/increasedchildhoodchronicjama_07.pdf

145) "Atopic dermatitis,"  Bieber T  N Engl J Med. 2008 Apr 3; 358(14):1483-94.

--  other data found in website of USA Today, posted 8/7/2005, "Allergy sensitivity doubles since 1970s," referring to August 2005 issue of the Journal of Allergy and Clinical Immunology,  found at  http://usatoday30.usatoday.com/news/health/2005-08-07-allergy-sensitivity_x.htm?POE=click-refer

 

145a) EPA, The Effects of Great Lakes Contaminants on Human Health, Report to Congress, Section III, p. 12 (bottom) and again on p. 16, at http://nepis.epa.gov/Exe/ZyNET.exe/2000BSHI.txt?ZyActionD=ZyDocument&Client=EPA&Index=1995%20Thru%201999&Docs=&Query=&Time=&EndTime=&SearchMethod=1&TocRestrict=n&Toc=&TocEntry=&QField=&QFieldYear=&QFieldMonth=&QFieldDay=&UseQField=&IntQFieldOp=0&ExtQFieldOp=0&XmlQuery=&File=D%3A%5CZYFILES%5CINDEX%20DATA%5C95THRU99%5CTXT%5C00000002%5C2000BSHI.txt&User=ANONYMOUS&Password=anonymous&SortMethod=h%7C-&MaximumDocuments=1&FuzzyDegree=0&ImageQuality=r75g8/r75g8/x150y150g16/i425&Display=p%7Cf&DefSeekPage=x&SearchBack=ZyActionL&Back=ZyActionS&BackDesc=Results%20page&MaximumPages=10&ZyEntry=20

 

146) see www.breastfeeding-and-asthma.info.  

 

146a) AAP Policy Statement on breastfeeding, at http://pediatrics.aappublications.org/content/129/3/e827.full#content-block

 

147) There was no entry for ADHD in the American Psychiatric Association manual until 1968,144 and the first data for ADHD prevalence (for the late 1990’s) showed it to include 6.5% of 5 to 17-year olds. But as of 2011-2013, 14% of U.S. boys age 5 to 17 had been diagnosed with ADHD.147 (CDC data at http://www.cdc.gov/nchs/fastats/adhd.htm) That figure is almost certainly much lower than the percentage in later school years separately, since a fourth of all ADHD cases are not diagnosed until age 9 and later.148

 

147a)  Lucas et al., Early diet in preterm babies and developmental status in infancy, Arch Dis Child. 1989 Nov; 64(11): 1570–1578.  PMC1792630, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1792630/

 

148) CDC, National Health Statistics Reports, Sept. 3, 2015, at http://www.cdc.gov/nchs/fastats/adhd.htm

 

149) Okada et al.,(2010), The ‘hygiene hypothesis’ for autoimmune and allergic diseases: an update. Clinical & Experimental Immunology, 160: 1–9, at http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2249.2010.04139.x/full

 

150) Type 2 Diabetes in Children and Young Adults:  A “New Epidemic”  Francine Ratner Kaufman, MD  CLINICAL DIABETES • Volume 20, Number 4, 2002  at http://clinical.diabetesjournals.org/content/20/4/217.full.pdf+html 

Also, a Univ. of Michigan article published in 2008 reported, “Recent studies suggest that there have been dramatic increases in type 2 diabetes among individuals in their 20s and 30s...." (at http://www2.med.umich.edu/prmc/media/newsroom/details.cfm?ID=422), which is compatible with origins of the epidemic in infant development after 1972.

 

150a) O'Neil and 7 others, Observational evidence and strength of evidence domains: case examples, Biomed Central: Systematic Reviews, at https://systematicreviewsjournal.biomedcentral.com/articles/10.1186/2046-4053-3-35

 

150b)  This can be verified by going to the websites of the AAP (American Academy of Pediatrics), AAFP (American Academy of Family Physicians) and ACOG (American Congress of Obstetricians and Gynecologists) and seeing their breastfeeding position papers.

 

151)  Simpson et al., A meta-analysis of the association between adherence to drug therapy and mortality, BMJ 2006; 333 doi: at http://www.bmj.com/content/333/7557/15

 

151a)  Yue et al., The effect of placebo adherence on reducing cardiovascular mortality: a meta-analysis, Clin Res Cardiol. <#> 2014 Mar;103(3):229-35. at http://www.ncbi.nlm.nih.gov/pubmed/24264475

 

152) Gary Taubes, Do We Really Know What Makes Us Healthy?  The New York Times Magazine, Sept. 16, 2007,  at http://www.nytimes.com/2007/09/16/magazine/16epidemiology-t.html?_r=0

 

152a) Type 2 Diabetes in Children and Young Adults:  A “New Epidemic”  Francine Ratner Kaufman, MD  CLINICAL DIABETES • Volume 20, Number 4, 2002  at http://clinical.diabetesjournals.org/content/20/4/217.full.pdf+html  Also, a Univ. of Michigan article published in 2008 reported, “Recent studies suggest that there have been dramatic increases in type 2 diabetes among individuals in their 20s and 30s...." (at http://www2.med.umich.edu/prmc/media/newsroom/details.cfm?ID=422), which is compatible with origins of the epidemic in infant development after 1972.

 

152b) American Diabetes Assn., Diabetes,  The Rise of Childhood Type 1 Diabetes in the 20th Century, Edwin A.M. Gale, Department of Diabetes and Metabolism, Division of Medicine, University of Bristol, U.K

 

152c)  Cited in The Future of Disability in America, Ch. 3, p. 77  Institute of Medicine (US) Committee on Disability in America; Field MJ, et al., ed.,  National Academies Press (US); 2007 bookshelf ID: NBK11437    found at www.ncbi.nlm.nih.gov/books/NBK11437

 

152d) CDC - MMWR National Surveillance for Asthma -- United States 1980-2004, Table 29, at www.cdc.gov/mmwr/preview/mmwrhtml/ss5608a1.htm

 

152e) Colen et al., Is breast truly best? Estimating the effects of breastfeeding on long-term child health and wellbeing in the United States using sibling comparisons, Soc Sci Med. 2014 May;109:55-65. doi: 10.1016/j.socscimed.2014.01.027. Epub 2014 Jan 29. at http://www.ncbi.nlm.nih.gov/pubmed/24698713

 

152f)  Figure 12.1 in SEER data at http://seer.cancer.gov/archive/publications/childhood/childhood-monograph.pdf

 

152g) Chapter 4, p. 53 of Clinical Guidance for the Health Conditions Identified by the Camp Lejeune Legislation (2015), at https://www.nap.edu/read/18991/chapter/6:    "...childhood cancers have latency periods of at least months....:"

 

152h) World Trade Center Health Program:   Minimum Latency & Types or Categories of Cancer, at http://www.cdc.gov/wtc/pdfs/wtchpminlatcancer2013-05-01.pdf

 

153) Curtis et al., Placebo Adherence, Clinical Outcomes and Mortality in the Women’s Health Initiative Randomized Hormone Therapy Trials, Med Care. 2011 May; 49(5): 427–435. at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4217207/

 

154) Stetler, Adherence, Expectations, and the Placebo Response: Why is Good Adherence to an Inert Treatment Beneficial?, Psychol Health. 2014 Feb; 29(2): at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3851940/

 

 

Remember from above that studies have observed that nursing infants consume a daily dioxin toxic equivalency that is 50 times that of adults;24a that is an effect of dioxin's being an organohalogen; organohalogens are lipophilic (attracted to fats), which causes them to become concentrated in breast milk.  Other organohalogens in breast milk (PCBs, PBDEs, and many pesticides) therefore also become concentrated in that milk far beyond normal environmental exposures.139f  Bear in mind that infant formula has been authoritatively found to contain essentially no detectable amounts of PCBs30 and pesticides,142, 143 and extremely little of dioxins75 and PBDEs. 55, 56

 

Approximately 12.3% of U.S. children are born preterm (gestational age < 37 weeks) (Hamilton et al. 2010)

 

"more than 90% of the total daily human exposure to PCBs and dioxin-like chemicals is made up of oral intake from food, whereas other routes (e.g. water, air and soil) contribute less than 10% of total exposure (Furst et al. 1992; Theelen et al. 1993),"  (Massart et al., Chemical Biomarkers of Human Breast Milk Pollution, Biomark Insights, Mar. 2008, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688366/

 

 An authoritative study determined that most of overall human PBDE intake in the U.S. was accounted for by exposures to dust. 118r (Remember from Section 2.a.1 that it was concentrations of household PCB dust, specifically, that were strongly related to distance from major roads.)