Development Problems of Male Children, in Relation to Breastfeeding




Introduction (summary):  Far more young males than young females have been diagnosed in recent decades with certain neurological impairments, including ADHD, learning disability 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.



Developmental exposures to certain environmental toxins (PCBs, brominated flame retardants, dioxins, and mercury) have been linked in many studies with later symptoms of various neurological impairments very disproportionately in young males. These specific toxins are all high in human milk and very low in the principal alternative infant feeding. The impairments discussed here have all been diagnosed with much greater frequency in recent decades, and rates of breastfeeding have also greatly increased in recent decades. (For the full text, including references to authoritative sources, see later)



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


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

Preview of Fig. 3

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



Section B.1 (summary):  In addition to the direct associations described above, these toxins have also been found to be linked with adverse neurological outcomes specifically in males via reduction of certain hormones, including testosterone. Testosterone has a major role in promoting neurological development and is also important to male motivation and attention. (Full text, including references to authoritative sources, at Section B.1)


Section B.2 (summary):  Effects of dioxins have been found to include testicular atrophy as well as reduction of testosterone levels.  Substantial evidence also indicates that attention deficits and long-term reduced motivation are likely outcomes of dioxin exposure. (Full text, including references to authoritative sources, at Section B.2)



Section B.3 (summary):  A 2014 American study found that a 10% increase in PCB levels in adolescent human males was associated with a 5.6% decline in their testosterone levels.  Observe in this chart the large increases in PCB levels that can occur during breastfeeding, with implications of resulting large corresponding reductions in testosterone levels.  (Full text, including references to authoritative sources, at Section B.3)


Section B.4 (summary):  PBDEs, also, affect male hormones including testosterone, with outcomes including hyperactivity.



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


 Preview of Figures 10 and 10.a


Section D (summary):  There is close historical parallel of increases in breastfeeding with births of males who will later have increasing problems associated with testicular dysfunction. This might not be coincidental, given the evidence about effects of toxins in breast milk as related to testicular atrophy and testosterone reduction. 


Declines in testicular function would be expected to lead to deficits in the male hormones that are important to attention and motivation.  (Full text, including references to authoritative sources, at Section D)





Environmental toxins in recent decades appear to have had effects especially on male children, who are very disproportionately diagnosed with neurological disorders as well as falling behind in education:

The very high ratios of males to females among children affected by the increasing neurological disorders (especially ASD and ADHD) 1. 2 have been basically unexplained.  Disproportionate problems among boys have also reached well into the general population, far beyond those with diagnosed disorders (see below), again with nothing but speculation as to the cause of this disparity.


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



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


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

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

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

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

 -- Boys Adrift: The Five Factors Driving the Growing Epidemic of Unmotivated Boys and Underachieving Young Men (2009) by Leonard Sax, MD, Ph.D.;3 favorably reviewed by the Journal of the American Medical Association. (Note that the central word in the title is not “trend” or “increase,” but something much more serious:  epidemic.)


A 2006 article in the New York Times, headlined “At Colleges, Women Are Leaving Men in the Dust,” refers to a “new emphasis on young men's problems” as indicated in magazine covers and talk shows at that time, and quotes the director of the Centers for Men and Young Men at McLean Hospital/Harvard Medical School as saying "They have a sense of lassitude, a lack of focus."4


Quoting from a 2013 article in The Atlantic, “…boys are languishing while girls are succeeding,” and College admissions officers were at first baffled, then concerned, and finally panicked over the dearth of male applicants....”5  Such problems are also widespread among the 34 countries of the Organization for Economic Co-operation and Development.6  An official of that organization referred in 2016 to “low achievement among boys, often combined with a lack of motivation….”7


There is considerable speculation as to why all of this has been occurring, but nothing has gotten past the level of conjecture.8


When seeking an underlying cause, it would be helpful to look for the approximate time when the adverse mental trend for boys and men may have originated, which is likely to have been during the boys’ early developmental periods; there is substantial evidence about vulnerability of early-postnatal mental development to toxins, as indicated in Figure 2 and Section 2.a at  One author stated in a 2000 Simon & Schuster publication, “In the late 1990s… articles about boys' educational deficits began to appear in American newspapers with headlines (such as) ‘U.S. Colleges Begin to Ask, Where Have the Men Gone?’"9  Since a typical college student would be approximately 18 to 23 years old, it would therefore be logical to look back from the late 1990's to the mid-to-late 1970’s for the birth years of the boys who would later have been at typical college age when those articles about boys' educational deficits began to appear. There is also other evidence, based on college completion data from the U.S. National Longitudinal Survey of Youth, which is compatible with this period as constituting the birth years of the males whose percentages were declining in the college scene in the late 1990’s. (see chart in reference 10)


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



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



(As a preliminary to what follows, it should be pointed out that, 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." 12  Note that PBDEs and dioxins are chemical relatives of PCBs.)


A 2009 study by seven Italian researchers (Colciago et al.11) investigated effects of developmental exposure of rats to PCBs, one of the toxins that are typically in high concentrations in human milk in developed countries, as discussed in Section 3 of  The PCB exposures of the rats were in doses that did not cause general toxicity in the animals

Fig. 1

After the rats reached adult age, a test of learning ability was conducted with four groups:  males and females that had been developmentally exposed to PCBs, and males and females that had not been exposed (control groups).  In the first step of that test, the rats stepped into a dark compartment and received a mild shock.


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




A 2016 experiment with rats indicated effects of low-dose developmental exposure to methylmercury, as follows:  The exposed rats displayed normal locomotion and motor coordination, but male rats had “learning disturbances” and “a predisposition to depressive-like behavior.”  The female rats showed no such changes.13 


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

Fig. 2


 (Source of chart, Figure 5 at


As indicated in the above chart, impulsive-like behavior (chart A) and memory and attention deficits (chart B) both increased dramatically in males following developmental exposures to the pesticide, but increased relatively little in females.


According to the authors, the doses of pesticide administered were "lower than the developmental no observable adverse effect level ...which is used by the Environmental Protection Agency to set allowable limits of pesticide exposure of humans;" those per-kilogram-equivalent doses were administered to female mice that would bear and nurse litters from which the mice to be tested would be drawn, and those doses that were equivalent to what is considered acceptable for one person were divided among their entire litters, before the offspring demonstrated the effects shown above.  The P values shown are a statistical indication that there is one or less than one chance out of 1000 that the adverse outcomes following developmental exposure to the pesticide, regarding male impulsiveness, memory, and attention, were results of chance.




The question obviously comes up as to whether these toxins have the same effects on humans that they had in the animal experiments.  With regard to pyrethroid pesticides, a 2015 study using human data (from the NHANES survey) found that boys with detectable levels of this pesticide were almost three times as likely to have ADHD as boys who had non-detectable levels of pyrethroids, while in girls the increase was less than one-fifth as high.14


Fig. 3

There is also ample evidence indicating that the other toxins discussed here, also, have distinctly male-adverse effects on humans.  See effects of mercury on males above, and effects of lead especially on males below.

Fig. 4


Also, see Appendix A for more studies showing specifically male-adverse effects of these toxins in both human studies and animal experiments.



Regarding the chemicals discussed here, it is relevant that typical exposures of human infants via breastfeeding have been in doses far exceeding the relatively safe doses established by U.S. government agencies (in the cases of PCBs and mercury);15, 16 or typical exposures of breastfed infants have at least been substantial (in the cases PBDEs, lead and many pesticides).17, 18  And authoritative testing has found little or none of those chemicals in contemporary infant formula in the U.S. (see Sections 3.g of


Significant adverse neurological effects of PBDEs on boys but not girls:


A study being published in 2018 found significantly poorer executive function among 8-year-old males with higher levels of PBDEs, and null associations in females.18a (Note the finding in a 2007 study 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.48)


Bear in mind that that the nervous system, including the brain, is part of what makes up the body weights that were found to be below average for PBDE-exposed boys in this study.  This study did not investigate neurological effects, but development of the brain could be even more likely to be curtailed by PBDEs than the rest of the body, considering that those chemicals are mainly known to the EPA to be neurodevelopmental toxins.23


Also be aware (from Section B below and Section 3.b of of additional evidence of neurological harm caused by background-level exposures to PBDEs and their chemical relatives, PCBs and dioxins, all of which are normally present in substantial concentrations in human milk.



Consider the EPA's statement, "the most sensitive outcome of PBDE exposure is adverse neurobehavioral effects following exposure during the postnatal period;"23a also be aware that there is major additional evidence of distinctly male-adverse effects of PBDEs (see Section B.4 later).  


Given the above, consider whether there is any reason not to see a likelihood of harm to neurological development of males, specifically, resulting from common exposures to PBDEs during the postnatal period.  Could this, together with the rapid increases since 1972 in transfers of PBDEs to developing infants, help explain why boys have been "falling behind in school and life"? (This quote is from the title of one of the several recent books on this theme, listed earlier in Section A.1)  The increases of PBDEs in the environment in recent decades have provided the first major part of the increased exposures being discussed.  Effects of these increases would have been greatly amplified by the increases in the predominant pathway for transfers of those toxins to infants -- breastfeeding; remember the 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;48 also see Figure 10a about increases that have taken place in this main pathway for PBDEs to infants.


Could the increasing exposures of infants to male-adverse, neuro-developmentally toxic effects of PBDEs also help explain why boys have been far more frequently diagnosed with autism and ADHD than girls?


Remember that the PBDE exposures that have been linked with adverse effects distinctly in boys were not measured in umbilical cord blood or serum; they were measured in breast milk from hundreds of U.S. mothers. 



Bear in mind that, as of now, there are no widely-accepted explanations for the origins of autism and ADHD (much less for why they mainly affect boys), or for the falling behind of boys and young men. Given the serious natures of these problems, there is extra reason to give careful consideration even to explanations that are outside the normal main stream, if those alternative explanations have good basis in scientific findings.




There have been several more studies that have found male-adverse neurological effects of the toxins discussed here, which are all high in human milk:  See Section B just below (Section B.4 regarding PBDEs) and Appendix A.




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




Section B


Section B.1:  Effects of these toxins on male motivation and attention via reduction of certain hormones:



As will be explained shortly, most of the toxins discussed here reduce levels of testosterone, which would clearly have effects mainly on males.  The importance of testosterone to male motivation and mental functions will therefore be explained here.  According to Dr. Edmund Sabanegh, chair of the urology department at the Cleveland Clinic in Ohio, testosterone “…keeps men running. Diminished mental clarity, motivation, drive -- all of these things can be related to low testosterone."24  A publication of the Endocrine Society, the largest organization representing professionals from the field of endocrinology, says essentially the same thing.25  As will be explained a little later, testosterone supply in youth and in adulthood, and its mental effects, are greatly influenced by effects of the toxins that are being discussed here.


A 1991 study arrived at findings indicating importance of testosterone to attention, another trait that is obviously also important to progress in education.  Quoting from that study, “Considerable evidence suggests that testosterone (has)… effects on attention in mammals.” And also, “reduction by testosterone of distractibility by irrelevant stimuli has been demonstrated in tests” in three different types of animals.26


Aside from their importance to motivation and attention, sex steroid hormones are also important to neurological development and male mental functioning in general:   According to one expert, "Sex steroid hormones play a role early in brain development…  A wide variety of neural processes are influenced by sex steroid hormones, including neurogenesis, …growth of the neuronal cell body… synapse formation….and neuronal excitability."27  (italics added)   According to another expert, ”Gonadal, adrenal, and thyroid hormones affect the brain directly, ….any agent that disrupts normal hormone secretion can upset normal brain development."28  Other experts on neurological development point to testosterone, specifically, for the way it "clearly affects brain development;" they refer to the "critical period for the testosterone organizational effect" that takes place when the brain is developing.29 (For substantial evidence that the human brain is very actively developing and vulnerable to toxins during the early months after birth, see Section 2.a of


Since testosterone is

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

2) a predominantly-male hormone, and

3) vulnerable to reduction by certain common environmental toxins (see Sections B.2 through B.4 below), to which infants have been very increasingly exposed in recent decades (Figures 6 and  7 above and 10a below),


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


Declines in testosterone and testicular function in recent decades:

A web page of the American Physiological Society refers to a study being published in 2016 (Skakkabaek and 13 others), by “a team of experts in reproductive medicine from Denmark, Finland and the U.S.” in which the authors observed lower levels of testosterone in men.”  The first author of the study was quoted as saying (in reference to recent signs of subnormal function of male sex glands), “I was surprised that we found such poor semen quality among young men ages 20 to 25.”30  A 2010 article by a researcher with the Centre for Reproductive Biology of The Queen’s Medical Research Institute, Edinburgh, UK, who is author or coauthor of 303 studies, refers to the high incidence of low sperm counts in young (European) men and evidence for declining sperm counts in recent decades.31   Separate studies were published in 2007 telling about declining testosterone or sperm counts in recent decades in the U.S.31a and in western industrialized countries.31b



Development of the male sex glands, which have reportedly been increasingly malfunctioning in recent years, is apparently greatly affected by male hormones during infancy.  Testosterone normally increases very significantly in males during the early months after birth;32 this is normally accompanied by a high rate of testicular growth at that time. This rapid early testicular growth is followed by relatively little growth until 5 years of age.32a  It is probable that proper development of male sex glands depends on the normal (that is, increased) supply of testosterone during those early months after birth.33  Relevant to that, reduction of testosterone is known to be an effect of three different pollutants that are authoritatively recognized to be at high levels in breast milk; see subsections to follow.  Bear in mind that breastfeeding rates had increased greatly in the 15 to 20 years leading up to the births of the young men who were later to have such diminished testosterone levels and semen quality. (See Figures 7 and 10a)



Section B.2:  Effects of dioxins, which have been found to include reduction of testosterone levels as well as testicular atrophy; long-term deficits in male neurological development, motivation and attention are likely outcomes.



According to a team of 13 researchers with the EPA, animal tests by at least two different research teams have indicated that dioxins were able to “impair testosterone synthesis,” among other effects.34   A CDC report accessed on the CDC website in April of 2016 says that dioxins have been demonstrated in studies of environmental and occupational exposures to have led to lowered testosterone levels in men; six studies were cited in support of that statement.  Further, it says that animal studies have demonstrated effects of dioxins including lowered testosterone levels and testicular atrophy.35 


With the above in mind, remember the findings that (a) at 11 months of age, dioxin toxicity-equivalent concentrations in breastfed infants had become about 10 times higher than in formula-fed infants;36 and (b) average dioxin concentrations were found to be still twice as high in breastfed young men in their twenties as in those who had been formula fed.37


Given the evidence above as well as the additional text to follow, there is ample reason to predict that long-term effects of breastfeeding could include reduction of hormones that are important to male motivation and attention.



Dioxin exposures via breast milk appear to harm male hormone supply in adulthood:  Dioxin's effect of reducing male hormones was illustrated in the case of accidental exposures in Seveso, Italy.  A study (by Mocarelli and 12 others)37a  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.  To help explain that outcome, note that, even 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; that was the case in both the exposed group and in the comparison group.37b It is very probable that, when those young men were taking in the toxins via breastfeeding while passing through their developmentally vulnerable infancies, the dioxin levels in the breastfed infants were even more outstandingly high than they were in later years.


It should be emphasized that this study strongly suggests that environmental exposures such as the above, which can and do occur in modern industrial societies, can either have or not have harmful effects on developing children depending on the feeding type received during infancy.  Lactation has a property, based on very substantial evidence, of concentrating environmental toxins in the process of transferring them to infants. (see just above and also Section 2.b of  Depending on their feeding type, infants can receive either

   (a) just the original, direct exposure from the environment, or

   (b) that original exposure plus a highly-concentrated second exposure via lactational transfers from their mothers.


The secondary exposures via lactation can have substantial long-term consequences that may not occur as a result of the primary exposures alone.


This study was investigating only reproductive outcomes, but bear in mind that testosterone is also important to neurological development, as well as to motivation and attention. (see beginning of Section B)


Continuing on the subject of factors that could specifically affect progress in education, a study found effects associated with common elevated levels of dioxins in a general human population:  learning disability and attention deficit disorder were found to be two and three times as high among children with common elevated levels of dioxins as among children with undetectable levels.38  That study did not investigate effects on males and females separately; but considering the above-indicated effects of dioxins in reducing the principal male hormone (testosterone), a hormone that is important to attention and neurological development, it is very likely that the education-related effects of dioxin would be found to be greater in males, if measured separately.


Also see Section D later for more about a link between increase in breastfeeding and a parallel decline in male reproductive capacities.



Section B.3:  Effects of PCBs regarding testosterone, including far greater effects in adulthood than in childhood:


A 2010 study states that several studies have reported “inverse associations between PCBs and circulating testosterone levels in men.”39  The study mentioned just below (published later) was in addition to the several earlier studies that had arrived at such findings.


A 2014 American study, by a team of six researchers who were authors or coauthors of over 160 studies among them, found that an increase of 10% in PCB levels in adolescent human males was associated with a 5.6% decline in their testosterone levels.40  If PCB levels in adolescence seem to be only remotely related to breastfeeding exposures, there is actually a very significant relationship:  Duration of breastfeeding has been found to be a significant predictor of child PCB levels even at age 14;41  also, 30% higher PCB levels were found among breastfed than among non-breastfed youths at age 10.42


Given that testosterone levels are significantly reduced in association with higher PCB levels, remember how far PCB levels can increase as a result of breastfeeding, depending on the duration of the breastfeeding (see Figure 4 at  Remember that, in addition to its importance to motivation and attention in adolescence and beyond, testosterone is also important during infancy for neurological development and probably also for development of the testicles. (see Sections B.1 and B.2)


In a 2001 experiment with rats (Kaya et al.43 ), developmental exposure to PCBs was found to result in reduction of testosterone, but with noteworthy differences according to time period.  In the lowest-exposure group (which was the group with greatest similarity to typical human exposures), reduction in testosterone stemming from effects of exposure to PCBs during infancy rose from 12% in infancy to 34% in adulthood.  Normal early development of the glands that produce testosterone in adulthood was probably disrupted by the exposure to PCBs during infancy.   (Remember that according to an authoritative consensus statement, "The concordance between human and animal neurotoxicity assessment is remarkable as demonstrated for lead, mercury and PCBs."12  


So it appears that the cognitive effects of developmental PCB exposures are likely to be so minor in young children as to go unnoticed, at that early stage, whereas they could be very substantial in maturity.  This sheds some light on the studies that have not detected adverse effects of the high levels of PCBs in breastfed infants, on the basis of testing of young children, at which point the authors confidently declare that breastfed children are not harmed by the (indisputable) major presence of PCBs in human milk.


Concerning the ultimate effects of the developmental PCB exposure in adolescence and adulthood, remember from the beginning of Section B that effects of reduced testosterone include reduced motivation and attention. 


Considering the above evidence of long-term effects of PCBs in reducing production of hormones that are important to male cognitive functioning, it may be worthwhile to remember the 2010 summary of studies indicating that PCBs had been found to be present in human milk in doses 63 to 270 times the minimal risk level established by the U.S. ATSDR;15 and that report should be seen in comparison with a study by U.S. scientists that found no detectable PCBs in all but one of 104 samples of infant formula.45


The apparent destructive effect of developmental PCB exposure on male learning ability, as found in the Colciago study described in Section A.2, may have been mediated by effects of PCBs on testosterone.



Section B.4:  Effects of PBDEs that are relevant to progress in education:


Remember from the beginning of Section B the importance of testosterone to male neurological development, motivation and attention, then note the following quote from a study by a pair of scientists who are authors or coauthors of a total of 148 published studies:  "…most PBDEs have antiandrogenic activity….  Some PBDEs have been found to inhibit … a key enzyme in the synthesis of testosterone…."46  More about effects of PBDEs, including in typical environmental exposures, of substantially reducing testosterone can be found in part C.2 of Appendix C of


According to a 2005 animal study, The exposure to low-dose PBDE-99 during development caused hyperactivity in the offspring…. The doses used in this study… are relevant to human exposure levels.47 (italics added)  


Considering the above, bear in mind the evidence in Section 3.b at about the effect of breastfeeding on a child’s PBDE levels, including the finding of a 2007 study that PBDEs were over six times as high in children who had been breastfed as in those who had been formula-fed even as late as age four.48



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


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


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



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


As indicated above in Section B, considerable evidence indicates that toxins that are at high levels in human milk can lead to reduced testosterone, which in turn is very likely an outcome that stems from broader testicular dysfunction, of kinds seen in Figure 10 just below. Bear in mind the CDC report stating that dioxins have been found to lead to testicular atrophy.35  The probable effects of low testosterone that we are discussing here (low motivation, inattention, and more) are by no means limited to childhood.

 ­Fig. 10                                                                                         Fig.  10.a


Figure 10 above shows substantial decline in major aspects of testicular function in Finnish men born after 1979; such declines have apparently been common in western nations in recent decades (see Section b.1).  Some studies have seen signs of general declines in testicular function among men born before the 1970’s, but those findings have been strongly debated.50





Remember (from Figure 10.a just above and Figure 7 earlier) that activity of the major pathway for chemicals that are toxic to testicular function (see Section B) has increased dramatically in the U.S. and western Europe in recent decades; and during those same approximate years when breastfeeding was greatly increasing,

   a) large numbers of boys have been born who have had problems in education (see Section A.1), and

   b) neurological disabilities and behavioral and learning disorders, also, have greatly increased among American children,55, 56 and those disabilities have been over twice as high among males as among females.2




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. a1a -  a2c


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  I will quickly correct anything found to be inaccurate.


For a more complete statement about the author and Pollution Action, please go to


Don Meulenberg

Pollution Action

Fredericksburg, VA, USA


a1) See and

a1a) The Surgeon General’s Call to Action to Support Breastfeeding 2011, p. 33, at

a2) Figure 2 in Guyatt et al., GRADE guidelines:  1. Introduction -- GRADE evidence profiles and summary of findings tables, Journal of Clinical Epidemiology, at

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

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://






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


In a 2016 Chinese study of postnatal exposures of human children to typical contemporary (organophosphorous) pesticides, strong adverse neurological effects were found in males, compared with little or no effects in females.  The male-to-female ratios for developmental delay in the motor area of children with higher concentrations of  two of the pesticide metabolites were about 150 to 1 and 50 to 1.  The adverse effects of postnatal concentrations of one pesticide on the social area of males was over five times greater than the similar adverse effect on females.52  


Effect of mercury on signal transmission within brains of males only:   A 2007 animal experiment (Coccini et al.53) tested the effects of two common developmental toxins on certain receptors (MRs) that are present in the brains of both humans and rats, which enable transmission of signals between neurons. According to the authors, “these receptors are known to play a major role in many central functions including higher cognitive processes….”  Methylmercury had an effect of causing long-term decrease of MRs in one major part of the brain in male rats only; and PCBs led to a (delayed) decrease of MRs in another important part of the brain, again in males only.


Effects of PCBs, at background-exposure levels, in distorting the structure of the male brain, with less or no effects in females:  A 2005 animal experiment (Nguon et al.54) exposed developing rats to PCBs in doses that the authors considered to be “likely to result in PCB levels comparable to PCB levels found in the blood of Belgian children” as well as similar to levels in the blood of children in a study carried out in the U.S. Great Lakes region.  Measurements were taken of the rats’ cerebella, which were of special interest because problems in the cerebella in human brains have been extensively associated with autism (see Section 4.a of; in the exposed rats on postnatal day 6, the sizes of the females’ cerebella were not affected by the toxins, compared with controls, but the cerebella of exposed males were reduced by 14.3%, compared with control males.  Another change in the brains that was measured in connection with the PCB exposure, alteration of “L1” proteins (which are present in both human and rat brains) was four times as great in male brains as in female brains. Remember that these distortions in the brain, affecting males very disproportionately, followed developmental exposures to PCBs that were comparable to exposures found among substantial numbers of contemporary human children. And bear in mind the extreme differences between exposures to PCBs of breastfed versus non-breastfed infants while the brain is developing (see Figure 9 above and/or Section 3.a at


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



1) Figure 4 in CDC, Vital and Health Statistics, July 2008, Diagnosed Attention Deficit Hyperactivity Disorder and Learning Disability: United States, 2004–2006  at, is just a small part of the evidence, for a generalization that is basically general knowledge.


2) 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, 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).”


3) at


4) Tamar Lewin: At Colleges, Women Are Leaving Men in the Dust, New York Times, July 9, 2006  at

Quoting from that article:  “the gender gap has moved to the front burner in part because of interest from educated mothers worrying that their sons are adrift now that it's a problem of white sons of college-educated parents.” The sociodemographic groups with the highest rates of breastfeeding are whites and college graduates.


5) at


6) The weaker sex:  Boys are being outclassed by girls at both school and university, and the gap is widening, The Economist, Mar 7th 2015, at


7) Is the gender gap in higher education widening?  by Dirk Van Damme, Head of the Innovation and Measuring Division, Directorate for

Education and Skills, at, Monday, January 11, 2016


8) Richard Whitmire, Why Boys Fail: Saving Our Sons from an Educational System That's Leaving Them Behind,  AMACOM. “…why so many boys arrive in twelfth grade unprepared for college work and why so many young men who do go to college drop out before earning degrees. Is it really because classrooms are feminized? Is it really because their minds were warped by video games? Is it really because mothers cut the apron strings prematurely?”  also, “the oppressive boy code and guy code,” and “the feminist-dominated teaching profession.”


9) Christina Hoff Sommers, The War Against Boys:  How Misguided Feminism Is Harming Our Young Men (2000) Simon & Schuster, Chapter 1, at





10a) Collaborative on Health and the Environment’s Learning and Developmental Disabilities InitiativeScientific Consensus Statement on Environmental Agents Associated with Neurodevelopmental Disorders, 2008, at


11) Colciago et al., Chronic treatment with polychlorinated biphenyls (PCB) during pregnancy and lactation in the rat, Part 2, Toxicology and Applied Pharmacology, May 2009, at


12) Collaborative on Health and the Environment’s Learning and Developmental Disabilities InitiativeScientific Consensus Statement on Environmental Agents Associated with Neurodevelopmental Disorders, 2008, at


13) Onishchenko et al., Developmental Exposure to Methylmercury Alters Learning and Induces Depression-like Behavior in Male Mice, Toxicological Sciences, Vol. 150, Issue 2, April 2016, at


14) Wagner-Schuman et al., Association of pyrethroid pesticide exposure with attention-deficit/hyperactivity disorder in a nationally representative sample of U.S. children, Environ Health, v.14; 2015 at


15) 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 

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.”


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


17) Damgard and eight others, Persistent Pesticides in Human Breast Milk and Cryptorchidism, Environ Health Perspect. 2006 Jul; 114(7): 1133–1138. Table 2, at


18) 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  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  


18a) Vuong et al., Childhood polybrominated diphenyl ether (PBDE) exposure and executive function in children in the HOME Study.  Int J Hyg Environ Health. 2018 Jan;221(1):87-94. Epub  2017 Oct


(19) 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  


20)  Hoffman et al., Lactational Exposure to Polybrominated Diphenyl Ethers and Its Relation to Early Childhood Anthropometric Measurements, Environ Health Perspect, DOI:10.1289/EHP201 at


21) In an October, 2016 search on Google Scholar for "WHZ", of the studies that came up on the first page, most were obviously investigating malnutrition.


22) Mollereau and 22 others, Adaptive preconditioning in neurological diseases – therapeutic insights from proteostatic perturbations, Brain Res. 2016 Oct 1; at

Also see about varying responses to toxins at:

 UC Davis: How PCBs May Alter In Utero, Neonatal Brain Development, ScienceDaily, April 14, 2009, at


23) In the EPA's Fact Sheet on PBDEs, the first example provided as to what exposure to PBDEs "causes" is neuro-developmental toxicity, in both the introductory highlights and in the main text.  See web page at

23a) 2009 EPA Polybrominated Diphenyl Ethers Action Plan at, p. 12


24) Quoted from WebMD web page at


25) See Table 1b of Bhasin et al., Testosterone Therapy in Adult Men with Androgen Deficiency Syndromes:  An Endocrine Society Clinical Practice Guideline, The Journal of Clinical Endocrinology & Metabolism, Volume 91, Issue 6, First Published Online: July 02, 2013. At


26)  R.J. Andrew: Testosterone, attention and memory, Conclusion of chapter 7, p. 186, in Patrick Bateson, Ed., The Development and Integration of Behaviour, 1991, Cambridge University Press,  which can probably be found on Google by doing a search for “testosterone effect on motivation concentration attention”  possibly at


27) Judy L. Cameron, Dept. of Psychiatry, Neuroscience, and Cell Biology and Physiology, University of Pittsburgh, in "Effects of Sex Hormones on Brain Development," Chapter 5 of Handbook of Developmental Cognitive Neuroscience, MIT Press, 2001, edited by Charles A. Nelson and Monica Luciana. Charles A. Nelson is Research Director, Developmental Medicine Center at Children's Hospital Boston, and Professor of Pediatrics and Richard David Scott Chair in Pediatric Developmental Medicine Research at Harvard Medical School. Selected pages can be found at no charge at or at’s website, doing a search including the above book title and “sex steroids.”


28)  McEwen, Steroid Hormones and Brain Development: Some Guidelines for Understanding Actions of Pseudohormones and Other Toxic Agents, Environmental Health Perspectives Vol. 74, pp. 177-184, 1987.


29) 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


30) from a web page of American Physiological Society: at


31) Sharpe, RM 2010, 'Environmental/lifestyle effects on spermatogenesis' Philosophical Transactions of the Royal Society B: Biological Sciences, vol 365, no. 1546, pp. 1697-1712., 10.1098/rstb.2009.0206 at


31a) Travison et al.,  (January 2007). A population-level decline in serum testosterone levels in American men. J. Clin. Endocrinol. Metab. 92 (1): 196–202. doi:10.1210/jc.2006-1375. PMID 17062768.


31b) Dindyal S (2007). The sperm count has been decreasing steadily for many years in Western industrialised countries: Is there an endocrine basis for this decrease?. The Internet Journal of Urology 2 (1): 1–21.


32) Auyeung et al., Prenatal and postnatal hormone effects on the human brain and cognition, Pflugers Arch - Eur J Physiol, 2013, at


32a)  Berensztein et al., Apoptosis and proliferation of human testicular somatic and germ cells during prepuberty: high rate of testicular growth in newborns mediated by decreased apoptosis. J Clin Endocrinol Metab. 2002;87:5113–8.


33) MacLeod et al., Androgen action in the masculinization programming window and development of male reproductive organs, Int J Androl. 2010 Apr;33(2):279-87. at


34)  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


 35) U.S. CDC:  Biomonitoring Summary, Dioxin-Like Chemicals: Polychlorinated Dibenzo-/p/-dioxins, Polychlorinated Dibenzofurans, and Coplanar and  Mono-/ortho/-substituted Polychlorinated Biphenyls, at 


36) Abraham et al., POP accumulation in infants during breast-feeding. Organohalogen Compounds 48:25–26 (2000), as reported in Infant Exposure to Dioxin-like Compounds in Breast Milk  Lorber et al., Vol.110 | No. 6 | June 2002 • Environmental Health Perspectives at


37) 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)


37a) 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

37b) 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)


38) 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  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).


39) Meeker et al., Exposure to polychlorinated biphenyls (PCBs) and male reproduction, Syst Biol Reprod Med. <#> 2010 Apr;56(2):122-31. doi:10.3109/19396360903443658, at


40) Schell et al., Relationships of Polychlorinated Biphenyls and Dichlorodiphenyldichloroethylene (/p,p’/-DDE) with Testosterone Levels in Adolescent Males, Environ Health Perspect v.122(3); 2014 Mar, PMC3948020, Table 2, at


41) Needham et al., Assessing Developmental Toxicant Exposures via Biomonitoring,  Basic & Clinical Pharmacology & Toxicology Doi: 10.1111/j.1742-7843.2007.00185.x, p. 106  at


42) Schell et al., Organochlorines, Lead, and Mercury in Akwesasne Mohawk Youth, Volume 111 | Number 7 | June 2003 • Environmental Health Perspectives, at


43) Kaya et al., Mixture of Polychlorinated Biphenyls on Sex-Dependent Behaviors and Steroid Hormone Concentrations in Rats: Dose–Response Relationship, Toxicology and Applied Pharmacology , Jan. 2002, at

Female rats were exposed to a mixture of PCBs that was similar in composition to that in human breast milk, beginning before mating and continuing to the day of birth of the subsequent litter. At birth, concentrations of PCBs in the brains of the offspring were much lower than in the mother rats; but after weaning, PCB levels in the offsprings’ brains ranged from two-and-a-half to five times the levels in the brains of the dams.(Bear in mind that this degree of concentrating of the toxin as part of lactational transfer to the infants is what happens when maternal toxins are shared among an entire litter of infants.) 


45) 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


46)  Costa and Giordano, Developmental Neurotoxicity Of Polybrominated Diphenyl Ether (PBDE) Flame Retardants,  2008  Neurotoxicology   National Center for Biotechnology Information,  at


47) 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


48) 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.)


50) R.M.Sharpe, Environmental/lifestyle effects on spermatogenesis, Philos Trans R Soc Lond B Biol Sci. 2010 May 27; 365(1546): 1697–1712. at


52) Liu et al., Adverse Associations of both Prenatal and Postnatal Exposure to Organophosphorous Pesticides with Infant Neurodevelopment in an Agricultural Area of Jiangsu Province, China, Environ Health Perspect, May, 2016,  DOI: 10.1289/EHP196, at


53) 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


54) Nguon et al., Perinatal exposure to polychlorinated biphenyls differentially affects cerebellar development and motor functions in male and female rat neonates, The Cerebellum, June 2005, Volume 4, Issue 2, at


55) Houtrow et al., Changing Trends of Childhood Disability, 2001–2011, Pediatrics Vol. 134 No. 3 September 1, 2014 at


56) Pastor et al., Diagnosed attention deficit hyperactivity disorder and learning disability:  United States 2004-2006, National Center for Health Statistics, 2008, at


 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  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).




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


79) WHO, Persistent Organic Pollutants:  Impact on Child Health, p. 6, at


 99) Summary Health Statistics for U.S. Children: National Health Interview Survey, 2012, Appendix III, table VI, at


99o1) Sobolewski et al., Sex-specific enhanced behavioral toxicity induced by maternal exposure to a mixture of low dose endocrine-disrupting chemicals, Neurotoxicology, 2014 Dec;45:121-30. doi: 10.1016/j.neuro.2014.09.008. Epub 2014 Oct 22, at


99u) See, Sections 3.c and 3.d)


99v) Pesticides in the Diets of Infants and Children, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C.  1993, p. 43 at 


99x) Li et al., Breastfeeding Rates in the United States by Characteristics of the Child, Mother, or Family:  The 2002 National Immunization Survey, Pediatrics, Jan. 2005, Vol. 115, Issue 1, Fig. 1 (from 2002 NIS) at



99z) Bose et al., Anthropometric characteristics and nutritional status of rural school

  children, The Internet Journal of Biological Anthropology, Vol. 2, No. 1 at


103e) Shakkebaek et al., Male Reproductive Disorders and Fertility Trends: Influences of Environment and Genetic Susceptibility, Physiol Rev. <#> 2016 Jan;96(1):55-97. doi: 10.1152/physrev.00017.2015, at 


103d)  Lesmana et al., Lactational exposure to hydroxylated polychlorinated biphenyl (OH-PCB 106) causes hyperactivity in male rat pups by aberrant increase in dopamine and its receptor, Environ Toxicol,2014 Aug;29(8):876-83. doi: 10.1002/tox.21815. Epub 2012 Sep 20, at


103f) 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


 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

 106b) Medical Dictionary for the Health Professions and Nursing © Farlex 2012