Increases in Child Disabilities Associated with Increasing Exposures to Specific Environmental Toxins, and Evidence for Causation



Introduction Part 1:  Widely-accepted infant care advice is substantially based on research that doesn’t deal with crucial male-female differences in effects, and/or states findings with dubious accuracy.



Introduction Part 2:  Emergence of behavioral and learning disorders as major conditions among U.S. school children beginning in late 1970’s, mostly with no known causes



Section A:  Increases in disabilities, which grew especially rapidly during the late 1970’s and the 1980’s, followed by slower increases.


Section A.1:  Initially rapid increases in disabilities

 Section A.2:  More gradual increases in disabilities 1997-2008



Section B:  Developmental toxins to which infants were exposed via an avenue that rapidly increased beginning in 1972, then slowed during the 1980’s.


Section B.1:  Specific toxins to which infants are widely exposed beyond safe levels

Section B.2 Trajectory of growth of the pathway by which those toxins are transferred to infants


Section C:  The 2000’s:  Increases of disabilities specific to sociodemographic groups, and parallel increases of toxic exposures, similarly specific to sociodemographic groups.


Section C.1:  Variations in toxic exposures parallel with variations in child disabilities


Section C.3:  Causal relationships?


Section C.4:  PBDEs rapidly increasing in Americans, and indicated by considerable evidence to be developmentally harmful


Section C.5:  Mercury toxic to development, and increases in its transfer to infants and its absorption


Section C.6:  BPA increasing substantially:


Section C.7:  Other toxins in human milk, probably also increasing in the U.S. environment



Section D:  Studies finding strong evidence of links between certain toxic exposures and neurodevelopmental harm



    Appendix A:  More on effects of BPA

    Appendix B:  Increased transfer, absorption and accumulation of mercury linked with type of infant feeding:

    Appendix C:  Lead effects, and some exposure declining while other exposure increases:

    Appendix D:  More on effects of PBDEs, and about reporting that overlooks adverse effects of postnatal exposures

    Appendix E:  Major increase in exclusiveness of breastfeeding at the turn of the century:

    Appendix F:  Apparently favorable effects of mercury on girls may not be actually favorable.

    Appendix G:   Additional evidence of contrasting harmful effects of environmental toxins, especially mercury and pesticides, on males versus females






     Introduction Part 1:  Widely-accepted infant feeding advice is substantially based on research that doesn’t deal with crucial male-female differences in effects, or states findings with dubious accuracy.


Autism, ADHD, and learning disabilities have all increased dramatically among U.S. children in recent decades; and all three of those conditions, as well as mental retardation, mainly affect male children.(a)  A 2011 study by an eight-scientist team, when referring to the predominance of boys among those with developmental disabilities, stated that they found this pattern to be “present for nearly all developmental disabilities.(a1)


In addition to those children specifically diagnosed with disorders, there is evidence (below) indicating that average male children, also, have been disproportionately included in the adverse increases in recent decades.  And there is good reason to think that something identifiable in the environment underlies these trends.



Below:  Outcomes following elevated exposures to one of the environmental toxins to which most infants and children have been increasingly exposed in recent decades


Fig. 1


When viewing these charts, bear in mind that they show outcomes for the general child population in a community with no known unusual exposure except for mercury resulting from fish consumption.



The source of these charts is a study carried out in the Seychelles (Davidson et al., 2010 b).  Postnatal exposures to varying levels of mercury appeared to have effects on children when tested at ages 9 and 17, as seen here.  The authors acknowledged “significant adverse associations” related to male children, as seen in these charts; but they also said that their “findings are sporadic and not consistent,” and that “this outcome does not constitute evidence of any pattern of associations between MeHg (methylmercury) and achievement.”  While reading those surprising words, including about lack of any pattern related to achievement, note that these charts are the only reports in this study that provided results for males and females separately.


 (It should be pointed out that the apparently favorable effects of mercury on females may not be favorable in the long run -- see Appendix F)



There is apparently a widely-held notion that postnatal exposures to environmental toxins are not significantly associated with developmental disorders.(c)   The above authors’ statements would seem to be an illustration of researchers’ only reporting findings that fit their preconceived ideas.  The prevailing belief in non-significance of postnatal exposures is perpetuated by research reports that (as in this case) unjustifiably fall into line with the expectations.  In addition to personal biases and their recognized effects, publication bias is also a widely-acknowledged problem in reporting of scientific research, as is reporting bias.c1 


Also, most health outcomes in children are reported for both sexes combined, rather than separately as in these charts.  If the results of this study had been reported in the normal (gender-combined) way, only very minor or insignificant effects of postnatal mercury exposure would have been apparent.  It is entirely likely that there has generally been a failure of studies to reveal the actual, serious effects of environmental toxins, due to problems such as mentioned above.


For additional evidence from at least eight studies plus another highly-authoritative source, indicating that environmental toxins, especially mercury, can have sharply contrasting effects according to gender, go to Appendix G.


So there is good evidence indicating that males, specifically, are adversely affected by at least one important environmental toxin; in contrast, females are either affected far less or else are affected in an apparently positive way, by some contemporary toxic exposure(s).  Therefore, because of the gender-combined mode of reporting that prevails in most studies, readers are likely to be receiving impressions that are very different from what would be seen with a more thorough examination of the data.


Another easily-found study provides additional illustration of the tendency of authors of studies to make reports that conflict with their own data, especially if so doing brings the study into alignment with prevailing beliefs.  In a study of developmental delay (usually a precursor of mental retardation) and its associations with PBDE concentrations in children, the authors repeatedly summarized the findings as “minimal” or “null,” despite the following (very inconspicuously placed) data:  higher PBDE levels among the developmentally delayed group in all eight specific PBDE species in a certain category; substantially higher PBDE concentrations among the developmentally delayed in the totals for all four percentile groupings above the lowest level; average 56%-higher PBDE concentrations among developmentally-delayed children compared with typically-developing children.  For much more detail, see Appendix D.


The lead authors of the above study and the Davidson et al. study were both authors of scores of studies.  There appears to be no reason to believe that this kind of misrepresentation of findings does not occur widely, with the main difference being that it is usually not easy or possible to detect the conflict between the written reports, as published, and the actual data.


To sum up the above: 

    Generally-accepted views about children’s vulnerability to environmental toxins may be inadequately informed, due to research reports that

  (a) inaccurately describe their findings in a way that unjustifiably conforms to the prevailing beliefs, and/or

  (b) obscure the actual effects of toxins by reporting only gender-combined results.




    The above is especially significant with regard to a toxin (mercury) to which infants are often exposed in doses that greatly exceed U.S. safety standards.(see Section B.1 below)


   The problem of research reports and publishing that improperly conform to pre-existing beliefs is a difficult one.  But recognizing and dealing with that problem is especially important if the goal is to find the causes of the neurological disorders that have been rapidly increasing without explanation.  People need to be (a) skeptical of research reports that basically echo the prevailing beliefs, and (b) open-minded toward evidence that contradicts those beliefs.




Introduction Part 2:  Emergence of behavioral and learning disorders as major conditions among U.S. school children beginning in late 1970’s

Quoting from a 2014 study in the journal Pediatrics, by a team that included six doctoral degrees within the group, “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.(1)  Similar observations, including a more precise estimate of the time when these disorders began to increase substantially, were included in a 2008 publication of the U.S. Center for National Health Statistics, as follows “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.”  (This statement was based on observations of pediatricians and educators as well as government statistics.)(2)  Note that three decades before 2008, the approximate estimated time of the beginning of the disability increases among school-age children just referred to, would have been in the late 1970’s . (Significance of that period will become apparent later.)



The causes of the vast majority of those disorders are unknown.(2a)


Very likely related to the above is a 2008 consensus statement, signed by 57 scientists, health professionals and researchers (with 49 doctoral degrees among them), as follows:  “Recognition of the contribution of chemical contaminants to learning and developmental disabilities has increased substantially in recent years as new evidence has emerged both about the ability of neurotoxic chemicals to interfere with brain development and the susceptibility of the brain to chemicals.”(3)



 Fig. 2

Section A:  Increases in disabilities, especially rapid during the 1970’s and 1980’s, followed by slower increases



Section A.1:  Initially rapid increases in disabilities:

This chart, published by the U.S. Department of Education and based on parents’ responses to surveys,(4) provides good evidence of major increases in handicaps that could have been originating among American children beginning in the 1970’s.  Since the data in this chart is for 15-to-17-year-olds as of 1987 and 2001, the crucial early developmental periods for this population would have been in the early 1970’s and the mid-1980’s.  Taking into account the 7% increase in births as of the later group, there were over 400,000 more American children born in 1984-1986 (a period of just three years) who would have disabilities as of ages 15 to 17, compared with what would have been predicted on the basis of data from the children born in 1970-1972.  (See the last data line, “All disabilities,” in this chart)  




Section A.2:  More gradual increases in disabilities 1997-2008:

A 2011 study in the journal Pediatrics by a team that included researchers with seven doctoral degrees among them found that, during the twelve years leading up to 2008, there was a 17% increase in developmental disabilities among U.S. children aged 3 to 17, based on parent reports. That increase led to a total of about 10 million American children with disabilities.(7)   The U.S. CDC concurs with this study’s findings.(8)  


Note that the increase described just above, although reaching a very large total number of children with disabilities, was actually a substantially reduced rate of increase compared with the increases in the 1970’s and 1980’s.  A CDC statement of 2008 also observed the reduced rate of increase in handicaps, reporting that the rate of increase in enrollments in special education for specific learning disabilities was not as rapid as it had been earlier, following the “marked” increases of the 1970’s and 1980’s.(9)




Section B:  Developmental toxins to which infants were exposed via an avenue that rapidly increased beginning in 1972, then slowed  during the 1980’s



Environmental toxins entering human milk during the last half century:

Remember the highly authoritative consensus statement in the introduction about environmental pollutants that could underlie increases in disabilities, then note the statement by two leading experts on developmental toxins (P. Grandjean and A. A. Jensen) who wrote the following in a 2004 article in the American Journal of Public Health:  “These substances (various developmental toxins) have caused contamination of human milk only during the last half century, and long-term health impacts are now being discovered.”(10) 


The toxins that have been greatly increasing in the environments and diets of the general populations of developed countries in the last half century or so have increased especially in their concentrations in human milk, since most of them accumulate in fat tissues, from which they are mobilized and excreted during lactation. 


Section B.1:  Specific toxins to which infants are widely exposed beyond safe levels, in human milk:   

According to highly authoritative sources (mostly U.S. EPA and the U.S. Agency for Toxic Substances and Disease Registry, or ATSDR), human milk in contemporary developed countries now includes four neuro-developmental toxins at levels significantly exceeding governmentally-established thresholds for safety, as follows:  

(a) dioxins, exceeding the EPA’s Reference Dose (estimated reasonably safe dose, or RfD) by scores to hundreds of times;(11) 

(b) PBDEs, normally well above and up to 20 times the EPA’s RfD;(12)

(c) mercury, typically in human milk at four times the maximum allowed by U.S. law in bottled water, but in many cases much higher than that;(13)

(d) PCBs, typically in concentrations about 20 times the maximum allowed by law in U.S. public water supplies.(14)


All four of the above developmental toxins are present in infant formula in concentrations less than 4% as high, and usually less than 1% as high, as their concentrations in human milk.(15)  And three of the above four are among the toxins to which Grandjean and Jensen were referring when they expressed concern about the dramatically increased contamination of human milk during the last half century.(10)  A document of the World Health Organization states, “There are some very strong datasets, for PCBs, showing that environmentally relevant exposures to these endocrine disrupting chemicals caused cognitive and behavioural deficits in humans.”15a   That same document, referring to the worldwide increases in reported prevalence of childhood neurobehavioral disorders in recent decades, said that “there is sufficient evidence to conclude that a number of factors, including environmental, contribute to the increases in autism spectrum disorders and other neurobehavioral disorders; the document went on to specifically mention strong cases for causality regarding just three toxins:  lead, methylmercury, and PCBs.



Section B.2:  Trajectory of growth of the pathway by which those toxins are transferred to infants:

The major increases in levels of the above-mentioned toxins in human milk during the last half century were only part of what makes the effects of those toxins significant.  Also important were the major increases that took place in percentages of mothers who were breastfeeding in the U.S. and most developed countries in the 1970’s; it went from unusual to common in the years after 1971; that upward trend is still continuing (although there was a pause during the latter part of the 1980’s).(16) (see the chart below)  Adding to the effects of the increasing percentages, exclusiveness of breastfeeding substantially increased in the first decade of the 2000’s.

Fig. 3




In the above chart, note the following:

a) The increases in breastfeeding at 6 months were rapid during the 1970’s and early 1980’s (increasing four-fold over that period), during the infancy years of an age group of children whose percentages of handicapped increased greatly in later years. (see “Section A.  Increases in disabilities,” above)


 b) Following that initial run-up in breastfeeding rates, there was a pause and then slower rates of increase, which is compatible with the recognized reduced rate of increase in child disabilities during the 1990’s and early 2000’s. (see “More gradual increases…) in Section A above)  


c) If 5 or 6 years are added onto the time when breastfeeding first started increasing rapidly (for breastfed babies to reach school age), that would end up at about 1978.  So 1978 would be about when effects of toxins increasingly ingested during the vulnerable developmental period of infancy could start becoming apparent in children’s school performance.  In relation to that year, remember from the introduction the significance of the late 1970’s, which was approximately when “behavioral and learning disorders emerged as major chronic conditions affecting the development of school-aged children.”(2)


It should be noted that apparently none of the above information about toxins in human milk, and about the increases in those toxins, is disputed.  The author of this article has written at least three times each to the World Health Organization and to three U.S. physicians’ associations that promote breastfeeding (the associations of pediatrics, family physicians, and obstetricians/gynecologists), presenting the content about toxins in breast milk, and asking how they could be confident that those toxins were not having harmful effects that outweighed the benefits of breastfeeding.  Not one reply has been received from any of those organizations, despite the facts that the questions presented were reasonable and brief, the toxicity information was based on highly authoritative sources (as cited), and the matter under discussion was of great importance to the health of millions of children.  Letters have also been sent to seven scientists involved in the area of neurodevelopmental disorders (the entire science team at the major organization, Autism Speaks) asking if they knew of any avenue of exposure, aside from breastfeeding, that widely transmits any developmental toxin to infants in doses authoritatively recognized to exceed established safe levels; of the three responses received as of several months later, none suggested any other such possible avenue for even one toxin.  Remember from above that typical human milk in developed countries contains four such toxins.




Section C:  The 2000’s:  Increasing disabilities specific to sociodemographic group, and parallel increasing exposures to toxins, similarly specific to sociodemographic group


Fig. 4


A 2014 study (Houtrow et al.), published in the Journal Pediatrics, by a team with six doctoral degrees among them, provided an important update on the information quoted above.  They drew on data from an NHIS survey that has been “the principal source of information for the Department of Health and Human Services to monitor health trends in the United States since 1957.”17


This team found an important and surprising recent development in the ongoing increases in disabilities.  Quoting from that study, “…between 2001 and 2011 we found a differential (greater) increase among more advantaged groups of children. This trend held whether advantage is measured by family income, parental education, or family structure.“  Those greater increases can be observed in this chart from that study.



There is another point to note while looking at this chart:  there were also greater increases at the lowest levels, compared with next levels above the bottom, as shown by the increases for the groups with less than high school education and with lowest family income  



Section C.1:  Variations in toxic exposures in parallel with variations in child disabilities:


Notice in the chart below, from the U.S. Surgeon General’s Call to Action to Support Breastfeeding, a pattern of breastfeeding exposure that is identical to the pattern of childhood disabilities in the chart above:  Breastfeeding and the disabilities increases are both at their highest at the highest level of education; both decline by steps from that top level, parallel with declines in educational level; and both turn back upward at the bottom, as the educational level continues downward.

Fig. 5



This linear-downward-then-uptick pattern is apparently not merely random variation. It applied in the chart above in all three breastfeeding duration categories in relation to education levels, especially in the longer-duration categories.  It also applied to disabilities in children in both of the categories in the Houtrow study in which socioeconomic advantage could be examined in a range of steps (income and education).  And it also applied in considerable other data (see below).


The long-standing, consistent nature of this relationship (linear-downward-then-uptick, in relation to education), as regards breastfeeding, is found in historical data provided by the CDC; this continuing pattern appears in their data about breastfeeding rates in relation to educational levels from 2000 to 2010 (2000 was the first year for which that data is provided); this applied to both 6-month and 12-month durations of any breastfeeding (20 data sets altogether).  Breastfeeding rates were highest at the highest educational level, then declined linearly at intermediate educational levels, then turned upward at the bottom educational level.19  There was one deviation from the normal linear path downward in parallel with lower educational levels; but there was no exception to the record of breastfeeding rates always being highest among college graduates, in all 20 data sets.  And these were clearly strong effects of educational levels on breastfeeding rates, as seen in the above chart.


The strength of this same pattern over many years in relation to disabilities is seen in the dramatic differences in the increases in disabilities that are shown in Figure 4 above, especially in the greater increases at the highest levels of advantage.  That chart incorporates data from children born as far back as 1984 (17-year-olds as of 2001) and as far forward as 2008 (3-year-olds as of 2011).  So data applicable to almost 199,000 children born over a 24-year period went into producing figures showing an increase of over 50% in disabilities in children of college graduates, essentially no increase at the high school graduate level, and moderate upturns from the downward trend of disabilities when reaching the bottom educational level.  The increases were especially outstanding at the top level of advantage in all three cases in which it was measured.  And they formed a top-to-bottom-then-uptick pattern that is distinctive, in both cases in which at least four separate levels were measured.


The pattern formed by increases in disabilities related to income levels is not as distinct as the pattern in relation to educational levels.  That is probably because of the changeable nature of family income; the same people fall into different family income categories at different times with changes in employment status (both voluntary and involuntary), muddling the differences that are related to type of person. 


The Houtrow authors justifiably found it surprising that increases in disabilities should be so outstandingly high at the highest levels of sociodemographic advantage in all three such categories (also including family structure).  In addition to the increases as stated in their study, greatly increasing disabilities among children of college graduates had already been going on for many years before the Houtrow study period:  between surveys in 1987 and in 2001, there had been a 62% increase in disabilities among American children of college graduates, as opposed to only a 34% increase in the total number of children of college graduates in the general population.  By contrast, there was only a 3% net increase per capita in average disabilities among children of parents at educational levels below college graduate.20


The authors of the Houtrow study speculated that the increases in reported disabilities among children of advantaged families during the 2001-2011 period may have resulted mainly from increased diagnosis and reporting, rather than from actual increases in disabilities.  It is relevant to remember (from just above) that there had also been very unusually great disability increases among children of college graduates going on well before 2001, in addition to the later increases.  Such large, long-continuing increases would seem to call for more explanation than merely increased diagnosis and reporting among advantaged parents.


That kind of reasoning also does not help explain the disabilities increases that occurred among children of families at the bottom sociodemographic levels.  Remember that the uptick at the bottom occurred in both demographic categories in which the disabilities were reported in a range of levels.


Perhaps it is worth considering the fact that there is an avenue of exposure that transfers four different developmental toxins to infants in concentrations that greatly exceed established safe levels, an avenue that (a) has been greatly increasing in the population in recent decades, (b) has been far higher among children of college graduates than among the general population in all 20 of 20 data sets that measured such data, and (c) has also been unusually high (compared with mid-level families) among children of parents with less than a high school education. (See Figure 5 and the text below it.)  


In addition to the data about breastfeeding in relation to educational levels, which is related to that according to income levels, breastfeeding rates are known to be far higher among married women than among unmarried mothers.21  Married women were the third category found in the Houtrow study to also have had far greater increases in disabilities among their children.


Section C.3:  Causal relationships?

It would be reasonable to assume that one or more causal relationships would probably be underlying the pattern described above; it does not appear to be a random occurrence.  It is likely that people who reach higher educational levels are generally more diligent at following establishment recommendations as to advantageous behavior, just as they were more diligent at doing schoolwork assignments; and clearly the establishment recommendations in the 2000’s have been in favor of breastfeeding.  From college graduate level down to high school graduate level, breastfeeding rates decline in parallel with declining educational achievement; for most people at lower levels, considerations such as the need to work, and to work in places with minimal accommodation to breastfeeding, become greater influences reducing breastfeeding than they are at the highest levels.  But at the very bottom sociodemographic level, the low cost of breastfeeding, and probably the incentive (in WIC food assistance programs) of better benefits when infants are breastfed, stimulate an upturn in breastfeeding rates at that lowest level.22 So it is not at all surprising that breastfeeding rates should decline from highest educational levels down to high school graduate level, and then turn back up again at the lowest level.


It is not as easy to come up with probable reasons for why disability increases should also follow this distinctive pattern of linear downward, then uptick at the bottom.  The authors of the Houtrow study offered an explanation that could apply at the highest sociodemographic levels:  increased parental attentiveness to symptoms, and better access to care, bringing greater likelihood of diagnosis in some cases.  But that does not help explain the concurrent greater increases in diagnoses also at the lowest sociodemographic levels; the authors (a sizable, impressive team) did not even attempt an explanation for what was occurring at the lowest levels. 


Absence of a plausible explanation of what has been causing the increases at the lowest sociodemographic level should increase the concern that there is something else taking place at the highest level, other than merely increased diagnosis and reporting.  That is especially the case considering the magnitude of the increase in reported disabilities (51%) in the highest educational category, over a ten-year period, in addition to a major increase before that study’s data.


It is not unreasonable to believe that some effect could be resulting from the developmental toxins in breast milk, since

a) breastfeeding was increasing substantially over the period preceding or during these increases in disabilities, increasing in exclusiveness as well as in percentages (see Figure 3),

b) breastfeeding percentages in relation to sociodemographics follow the same unusual (linear-downward-then-uptick) pattern that was followed by the increases in disabilities (see Figure 5 and text below it); and

c) there is no dispute that typical human milk contains four different developmental toxins (known or strongly suspected) each of which is typically present in doses greatly exceeding established levels. (see Section B)


In relation to the possibility of a causal relationship in the above regard, see Section D below about peer-reviewed scientific studies that have found associations between exposures to those toxins and adverse developmental outcomes.  And remember from Sections A and B that the high and low increases in developmental disabilities in the U.S. before the 2000’s were preceded by corresponding high and low increases in U.S. breastfeeding:  (a) the emergence of child disabilities in the late 1970’s followed the rapid increases in breastfeeding by an interval that was very compatible with the infants’ reaching school age before disabilities were diagnosed; and (b) the time of the slower increases in disabilities was compatible with the time of slower increases in breastfeeding.  In addition to the parallels over several decades, the distinctive pattern of the increases in child disabilities in relation to sociodemographics (linear downward, then an uptick), as reported in the 2000’s, matches the pattern of breastfeeding rates in relation to sociodemographics.



Bear in mind that, after significant inquiry among qualified scientists, nobody has been able to suggest any avenue of exposure, other than breastfeeding, that widely transfers any developmental toxin to infants in doses recognized to exceed established safe levels. (see end of Section B.2)  Breastfeeding transfers four such toxins to infants.(see Section B.1)  Neither those scientists nor anybody else has disputed the above.


The increases in disabilities are sufficiently serious, and their continuing increases are so in want of explanations, that it justifies looking seriously at all plausible sources of toxic exposures, including sources that are widely believed to be beneficial. 


Of all the disorders that are said by the U.S. Surgeon General to be reduced by breastfeeding, all but one has actually substantially increased in the U.S. since breastfeeding greatly increased, after 1971; in the case of that one disorder that did not increase, neither was it reduced following the major increases in breastfeeding.23  Although various studies have found desirable effects to be associated with breastfeeding (always with known confounders present24), over 50 scientific studies have found breastfeeding to be associated with worse health outcomes.25   Among those was the study that was apparently the only study on effects of breastfeeding on childhood obesity that was randomized, which is the recognized best way to avoid effects of the confounders that often cause false conclusions in typical studies. 




For the U.S. generation born in the mid-20th century, breastfeeding was unusual.  That generation did not have the unexplained childhood epidemics and major increases that have become prevalent since then:  diabetes, asthma, allergies, obesity, autoimmune disease, ADHD and autism.  In the decades since 1971, there have been not only major increases but also lows and mid-levels of multiple childhood disorders that have correlated closely with preceding increases, lows and mid-levels of breastfeeding rates.(see and, with many authoritative sources cited at both websites.)  There are many other well-substantiated, authoritative reasons to doubt the popularly-accepted view about benefits of breastfeeding.25




(Unfortunately, data for breastfeeding broken down by socio-demographic groups is not available for the years before 2000; but the post-2000 years are the most important ones for discussing effects on child disability increases after 2000, since by far the greatest increases in disabilities were among children below age 6. (See Figure 4 above.) )



Not only has this uniquely major avenue of infant exposure to developmental toxins been increasing and varying in close parallel with the varying increases in child disabilities, but levels of two toxins transferred via that avenue have also been increasing dramatically. (see below)  Levels of other serious developmental toxins have been at least stable in the environment, if not increasing, while their transfer to infants has been increasing.



Section C.4:  PBDEs rapidly increasing in Americans, and developmentally harmful, as indicated by considerable evidence:


The bio-accumulative PBDEs, with their endocrine-disrupting, anti-androgenic effects, and linked to neurodevelopmental harm, are found in breast milk in the U.S. in high concentrations:

a) remember that PBDEs in human milk have been reported (in EPA data and other authoritative findings) to be normally well above and up to 20 times the EPA’s RfD;(12)

b) at levels 10 to 100 times as high as in Europe,26  

c)  as of an authoritative 2007 report, "during the last 30 years, PBDE levels in humans have doubled about every 3 to 5 years and continue to increase."   A study of sediment from multiple locations in the Great Lakes found an increase of PBDE levels by a factor of several hundred times since the 1970s.27


According to a 2014 review of other 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.”28  According to a 2008 EPA report on PBDEs, "The animal model indicates a potential for concern for early lifetime exposure (i.e., fetal or infant exposure) to the chemical. The identification of BDE-99 in human maternal and cord serum, milk and children’s serum .... implies humans are exposed to BDE-99 (one form of PBDE) during a period of rapid development of the brain, a critical window of development, indicating a potential for susceptibility."29  (For information about the first year or two after birth being a period of rapid development of the brain, and of vulnerability to toxins, see Section 4 In a 2012 study cited by the NIH, "Exposure to (PBDEs) was associated with a higher risk for physical and mental impairment when children reach school age.  We observed associations of in utero and/or childhood exposure to these flame retardants and fine motor coordination, attention and IQ in school-age children." 30  Similar findings were stated in other studies.31 


A 2011 California study of associations in young children between PBDE concentrations and developmental delay (a prevalent and increasing condition that usually leads to later diagnosis of mental retardation) found that children with developmental delay had a mean 56% higher level of lower-brominated PBDEs than typically-developing children. (See Appendix D)


A 2012 study, of effects of PBDEs in breast milk, found that children who had consumed breast milk with first and second quartile levels of the predominant form of PBDEs showed over three and two times the likelihood of later having ADHD, based on behavior test scores, compared with children who had consumed breast milk with below-median levels of PBDEs.32  A 2011 study found that 4-year-olds with higher levels of PBDEs linked with breastfeeding history had an 80% increase in relative risk of attention-deficit problems and a 160% increased relative risk of poor social competence. (Note that poor social competence is one of the basic characteristics of autism/ASD.) This study found that gestational exposure to PBDEs in the mothers in the study had no significant adverse effect, but exposure to those same mothers' PBDE levels via breastfeeding did have substantial effects.33  This should be seen in combination with the nearly 3-to-1 difference in levels of PBDEs in breastfed as compared with formula-fed children at age 4, as reported in what is apparently the only study that has made such a comparison.34   (The above is compatible with authoritative reports of breast milk concentrations of PBDEs (a persistent toxin) being over 30 times those in infant formula.35) These substantial effects should also be seen in light of the fact that the above study was carried out in Europe, where exposures to PBDE levels are many times lower than in the U.S.  The findings of effects of PBDEs in studies of humans have been confirmed by similar effects in animal studies carried out under controlled conditions, including with concentrations ingested by the animals in levels not far above those found in human milk.


Given the above links between PBDEs and adverse neurological development, it is of relevance that breast-fed infants have been estimated to be exposed to 306 ng/kg body weight/day PDBE compared with 1 ng/kg body weight/day in adults.36  For more information about PBDEs in human milk, see Section 1 of



Section C.5:  Mercury toxic to development, increasing in the U.S. food chain in recent decades, and increasing in its transfer to infants and its absorption:  


According to an authoritative 2004 review of the scientific literature on this topic, “Although Pb (lead) is perhaps the most publicized and well known of the pediatric metal intoxicants, Hg (mercury) is probably at least equally toxic if less well known.”37   A document of the World Health Organization, discussing the worldwide increases in reported prevalence of autism and other childhood neurobehavioral disorders in recent decades, referred to “strong” causal evidence regarding methylmercury in relation to the increases in the autism;15a strong causal evidence in relation to autism was mentioned in reference to only two other toxins (lead and PCBs).  (For considerable specific information on neuro-developmentally toxic effects of mercury on infants, see  Remember from the Introduction Part 1 the evidence that the general male child population, not merely those with diagnosed disorders, is also adversely affected by mercury; as also indicated there, the usual gender-combined data would greatly understate the effects on males specifically. of twelve scientists and physicians with impressive credentials stated in a 2006 document, “research shows that mercury levels in the food chain are increasing, with the greatest concern focused on popular fish such as swordfish and tuna.”38  (Increases of mercury in popular seafood are especially significant because consumption of fish is considered to contribute almost half of the mercury concentrations in the U.S. population.)  According to FAO statistics, U.S. per capita consumption of fish and seafood increased 74% between 1970 and 2005.38a  According to a web page of the U.S. National Oceanographic and Atmospheric Administration, 91% of seafood consumed in the U.S. is imported, and about half of it is farmed; of the six kinds of seafood most consumed in the U.S., the predominant sources are China and its neighbors.39  Atmospheric mercury emissions from Asia, especially from China, have been by far the largest in the world in recent decades and have been rapidly increasing.40   Evidence indicates that levels of two (of the several) species of mercury in U.S. women of childbearing age were stable rather than rising during the first decade of the 2000’s -- possibly due to diet modifications following publicity about mercury in fish -- but the period of infant exposure that would be relevant to the Houtrow study goes back to 1983.41

But, aside from increases in maternal mercury levels since 1983, total transfers of mercury to infants would also have increased greatly during that period, given the amount of mercury in breast milk (see Appendix B.1) combined with the increases in both breastfeeding rates (Section B.2) and exclusiveness of breastfeeding (Appendix E) that were taking place.  As just part of the evidence:  in a study by a prominent scientist (P. Grandjean) and his team, it was found that total mercury concentrations in infants that had been breastfed for one year were three times as high as those in infants that had not been breastfed.42  And, once ingested, metals (including mercury) become absorbed and accumulate far more efficiently when the infant is consuming a milk diet, such as has become much more prevalent in recent decades. (see Appendix B, item 2.)  The tripling of mercury in an infant body linked with a year of breastfeeding almost certainly greatly understates the resulting concentrations in the brain, since the half life of mercury in the body is about 60 days, whereas it is estimated to be as long as 20 years in the brain.42a



Section C.6:  BPA increasing substantially:

People are exposed to BPA largely from its use in polycarbonate plastics and in linings of food packaging, including canned goods.  There are many reasons to consider BPA to be developmentally toxic (to follow); and it was rapidly increasing in the environment during the years of the births of the children whose increasing disorders were reported in the above study.  U.S. production volume of BPA increased from one billion pounds in the early 1980’s43  to  2.4 billion pounds in 200744, which implies a very major increase in BPA production during the years of the births of the children whose disorders greatly increased during the period studied, as reported in the Houtrow study.


The Canadian government has declared BPA to be a hazardous substance, the European Union has banned BPA for use in baby bottles,45 and the U.S. EPA states, “BPA is a reproductive, developmental, and systemic toxicant in animal studies and is weakly estrogenic, there are questions about its potential impact particularly on children’s health…. “46  A web page of the U.S. National Toxicology Program quotes the Program’s associate director as stating, “the studies in animals (of BPA effects) have shown a variety of effects at very, very low levels.47   According to a 2013 study by a five-scientist team, “Many studies have also reported BPA effects on the development and function of the central nervous system (brain and spinal cord),” specifically including effects on a part of the brain (locus coeruleus) that is thought to be important to attention, emotion, motivation, learning and memory.48   For considerable additional evidence concerning effects of BPA on neurological development, including in leading to inattention and hyperactivity behaviors and reducing testosterone, see Appendix A.


 A 2013 study of BPA in early breast milk of 325 lactating women estimated breastfed infant BPA levels to be about 10 times those of adults, and found the median level of BPA in colostrum to be 7.8 ng/mL.49  Results of testing for BPA in liquid infant formula, as published in a 2008 study (measured well before BPA was banned from formula packaging in 2013), found BPA to be present in an average concentration of 2.88 ng/g.50  So, even before BPA was removed from formula packaging, its BPA levels were less than 40% of the BPA level in early breast milk as found in the study quoted just above.


The weighted mean of the data for BPA concentrations in amniotic fluid as found in two studies (published in  2010 and 2013) was 1.27 nanograms per ml, and the weighted mean for the concentrations in breast milk was 6.1, indicating five times greater exposure via lactation than via the transplacental route.51



Section C.7:  Other toxins in human milk, probably also increasing in the U.S. environment:


Dioxins:  Dioxin emissions from diesel combustion in the U.S., according to the most recent EPA reports, appear to have roughly doubled between 1987 and 2000.52  Emissions from smokestack sources have declined greatly, but those emissions would typically rise high from stacks and keep rising for some distance due to their heat, and then drift great distances (typically hundreds of miles) before settling to earth,53 mostly well outside urban areas; this contrasts with diesel emissions, which are to a large extent emitted at or near ground level, in more densely-populated areas, from trucks, buses, trains, ships, dredging and other port equipment, construction machinery, etc..  Judging by the most recent data on dioxins in breast milk (as provided in this chart), dioxins have been increasing in U.S. breast milk.  (Note that the darker dots represent data for the U.S.)


PCBs:  PCBs in U.S. breast milk declined sharply from the late 1970’s to 1982, but the only data that seems to be readily available for after 1986 indicates a gradual increase in the U.S. since then.54   It should not be surprising that PCBs are increasing in the environment even well after most intentional production of PCBs was ended; they are known to persist in the environment, leaking from old electrical equipment and old caulking in buildings, and they are products of ongoing (usually increasing) combustion; according to a web page of the NIH, PCBs are by-products from most forms of burning, including industrial burning, automobile exhaust, and wood or trash burning.55




Section D:   Studies finding strong evidence of links between toxic exposures of interest here and neurodevelopmental harm:


Autism-related effects of relatively commonly-present concentrations of these toxins:  

At least five published studies have found high levels of mercury in people with autism.56  (The studies that have failed to find this association have (a) focused on thimerosal, which contains only ethylmercury, one of many species of that chemical, (b) measured mercury levels in children far past the vulnerable early-postnatal period), and/or (c) obscured the effects of mercury on males by reporting data for both sexes combined. (see Introduction 1 about how misleading that can be.) The studies finding associations of autism with mercury levels less than twice the normal range should be seen together with the findings in multiple studies of doubling or tripling of infant mercury levels resulting from breastfeeding, taking place during the infant’s period of rapid brain growth.57


A major 2013 study, analyzing data from all over the U.S., found close associations between autism prevalence and exposures of the mothers to variations of air pollution of kinds very widely present across the U.S., especially diesel emissions.58

Note that diesel emissions include dioxin, PCBs and PBDEs, and that these toxins are passed on to a breastfed infant in greatly concentrated form -- see below.


Such studies have sometimes been interpreted to mean that harm results from fetal exposure to toxins during gestation, but close reading of the studies reveals nothing indicating that the harm was necessarily prenatal. The effects were at least as likely to have originated from postnatal exposures, as indicated by the following:   two leading experts on toxins involved in child development (P. Grandjean and P.J. Landrigan) have stated that “Persistent lipophilic substances (which include dioxins, PCBs and PBDEs), 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.59    So high levels of toxins, accumulated from the mother’s long-term exposures, are steadily ingested by a breastfed infant during the continuing period when the brain is especially vulnerable to toxins due to its rapid growth and development.  For much more on this topic, see


Related to the above:  On the basis of data from all 50 states and 51 U.S. counties, a highly-published scientist and Fellow of the American College of Nutrition found that "exclusive breast-feeding shows a direct epidemiological relationship to autism" and also that "the longer the duration of exclusive breast-feeding, the greater the correlation with autism."60  Another U.S. study, a Canadian study, and a U.K. study all arrived at compatible findings; and all of them in combination indicated that greater likelihood of autism was linked to greater duration of breastfeeding. (For details, see Appendix 2.a at


For considerable other information on correlations between lactational exposures to toxins (especially mercury) and subsequent incidence of developmental disorders, see


Increases in breastfeeding exposures during the first 10 years of the 21st century might not at first  appear to be large enough to account for some of the increases in children’s mental disorders, until one understands about the increases in exclusiveness of breastfeeding that took place at the turn of the century, along with the increases in percentages breastfed.  See Appendix E



There is a widespread notion to the effect that prenatal (as opposed to postnatal) exposures to developmental toxins are the only exposures that significantly affect the brain’s development.  That idea is based on evidence that is valid with respect to certain toxins and certain types of brain defects but not with respect to others, according to the highest scientific authorities and according to many scientific studies.  For considerable information on this topic, go to 



Comments or questions are invited.  At the next link are comments and questions from readers, including a number of doctors.  Some of the doctors have been critical but at least four have been in agreement with us, including two with children of their own with health problems and one who says she has delivered thousands of babies; they put into briefer, everyday language and personal terms some important points that tend to be immersed in detail when presented in our own publications.  Also, we have responded to many readers’ questions and comments, including about having breast milk tested for toxins and about means of trying to achieve milk that is relatively free of toxins, including the “pump and dump” option.  To read the above, with a link for sending your own comments or questions, go to   If you have criticisms, please be specific about any apparent inaccuracies, rather than merely saying you don’t like what is said here.  Note that we don’t feel obligated to present the favorable side of the breastfeeding debate, since that is already very amply (and one-sidedly) presented in many other, widely-distributed publications as well as in person by numerous enthusiastic promoters. 


*To read about Pollution Action and the author of this article, go to




Index to Appendices

Appendix A:  More on effects of BPA

Appendix B:  Increased transfer, absorption and accumulation of mercury linked with variation in infant feeding:


       1) Transfer of mercury according to type of feeding

       2) Absorption and accumulation of mercury according to type of infant feeding



Appendix C:  Lead effects, and some exposure declining while other exposure increases:

          Continuing lead exposure of many infants


Appendix E:  Major increase in intensity of breastfeeding at the turn of the century:


Appendix F:  Apparently favorable effects of mercury on girls may not be actually favorable:


Appendix A:  More on effects of BPA

 According to a 2010 study by a six-scientist team, “Published results have demonstrated that perinatal exposure to levels of BPA below the no-observed-adverse-effect level (<50 mg/kg/d) affects the neocortical histogenesis (formation of tissues in the site of most of the higher brain functions), sexual differentiation of the brain, and behaviors in the offspring of rodents.”  (Xu et al., Perinatal exposure to bisphenol- a changes n-methyl-d-aspartate receptor expression in the hippocampus of male rat offspring, Environmental Toxicology and Chemistry, Vol. 29, No. 1, pp. 176–181, 2010, at  Sexual differentiation, with the accompanying effects on testosterone production that have been found, is relevant to general mental development because (according to a medical school research team) "Hormones as mediators of gene effects control indirectly the development of human body and brain, with subsequent consequences on behavior and cognitive functions.....A number of published studies documenting the relationship between testosterone and human intellectual performance have indicated that testosterone exerts its effects neuroanatomically by influencing the organization of the developing brain, modifying cognitive pattern ." (emphasis added)   (Intelligence and salivary testosterone levels in prepubertal children  Ostatnıkova et al., Institute of Physiology, School of Medicine, Comenius University, Bratislava, Slovak Republic  Neuropsychologia 45 (2007) 1378–1385   Elsevier  at


A 2007 review of evidence about BPA effects, provided by a team of nine scientists, reported “There is extensive evidence” based on “multiple independent studies” indicating that exposure to low doses of BPA during critical periods of development “have persistent effects on brain structure, function and behavior in rats and mice.”  They specifically pointed out anti-androgenic and anti-thyroid-hormone effects.  They cited eleven studies in support of the observation of BPA’s having effects on one sex but not on the other, and another four studies finding effects of BPA in leading to early onset of puberty in females, which they say is “ linked to postnatal growth.”  They also reported that numbers of certain cells in testes of young males were significantly reduced by BPA exposure, and testosterone in adults was “dramatically reduced” by low-dose BPA exposure. (Richter et al., In Vivo Effects of Bisphenol A in Laboratory Rodent Studies, Reprod Toxicol. Author manuscript; available in PMC 2008 Aug 1, Published online 2007 Jun 26. doi:  10.1016/j.reprotox.2007.06.004, PMCID: PMC2151845 at; for similar findings in a 2014 study, also see Mileva et al., Bisphenol-A: Epigenetic Reprogramming and Effects on Reproduction and Behavior,  Int J Environ Res Public Health. 2014 Jul; 11(7): 7537–7561. Published online 2014 Jul 22. doi:  10.3390/ijerph110707537  PMCID: PMC4113893 at  (Remember from the BPA increasing section in the main text that sex hormones are known to affect neurological development, including organization of the brain.)  There have also been a number of studies that have found no effects of BPA, but this group pointed out that “The major factor that accounts for 13 studies that draw the conclusion of no effect of low doses of BPA is the use of a (specific) strain of rat” that had been selectively bred and that has been found to be insensitive to certain chemicals such as BPA.


Before reading about the following effects of BPA in children, note the authors’ statement that BPA concentrations in the population investigated in this study were considerably lower than in the general U.S. population.    “Our study and Maserejian et al both found BPA exposure in childhood to be associated with anxiety and depression in boys and girls. Maserejian et al found additional associations with personal/clinical maladjustment and emotional problems while we found childhood urinary BPA concentrations were associated with increased scores for … depression (β = 1.2; 95% CI: 0.3, 2.2), hyperactivity (β = 1.1; 95% CI: 0.0, 2.1), and inattention (β = 0.9; 95% CI: 0.3, 1.5) on the BASC-2.  Childhood urinary BPA concentrations were associated with increased externalizing behaviors, including conduct problems, in girls at age 7 and increased internalizing behaviors and inattention and hyperactivity behaviors in boys and girls at age 7….  biological mechanisms exist to support the findings observed in this study.”  (Harley et al., Prenatal and Early Childhood Bisphenol A Concentrations and Behavior in School-Aged Children, Environ Res. 2013 Oct; 126: 43–50.  Published online 2013 Jul 17. doi:  10.1016/j.envres.2013.06.004  PMCID: PMC3805756 at


“Immune function, enzyme activity, brain structure, brain chemistry, and behavior are all affected by exposure to low doses of BPA.  Such effects have been found of exposures during lactation and post-weaning, in animal experiments.  …  Behavioral effects include hyperactivity… and increase in aggressiveness    94% of government-funded studies have found adverse effects of low-dose exposures to BPA.  Low-dose exposure to BPA (at or below the RfD) has been found to block synthesis of testosterone (vom Saal et al., An Extensive New Literature Concerning Low-Dose Effects of Bisphenol A Shows the Need for a New Risk Assessment, Environ Health Perspect. 2005 Aug; 113(8): 926–933. Published online 2005 Apr 13. doi:  10.1289/ehp.7713   PMCID: PMC1280330  at


“It is evident that BPA can cause adverse effects in animals at doses several orders of magnitude lower than not only LOAEL but also the reference dose, …Overall, the emerging data suggest that BPA exposure alters activity within the immune system and these effects may be most evident and persistent when BPA exposure occurs during early development. The known interactions between immune function and brain development may be an important consideration in studies of BPA-induced effects …There is also evidence that BPA may have anti-androgenic activity….”  (Kundakovic et al., Epigenetic perspective on the developmental effects of bisphenol A, Brain Behav. Immun., 2011 Aug;25(6):1084-93. doi: 10.1016/j.bbi.2011.02.005. Epub 2011 Feb 17.  at


According to the CDC, “In animal and human studies, bisphenol A is well absorbed orally. …  recent animal studies which suggest possible low dose effects include … inhibition of postnatal testosterone production, and changes in neurodevelopment.”  (CDC Biomonitoring Summary:  Bisphenol A, CAS No. 80-05-7 at


“Thirty infants (55%) were exclusively fed breast milk, 24 (44%) were exclusively fed formula, and 1 received a mixture of breast milk and formula…. Two breast milk samples had concentrations of… BPA that were at least 1 order of magnitude higher than the concentrations in other nutritional samples…. These 2 statistical outlier samples were not included in further analyses.”<<two out of 31 deleted, which would have greatly raised the breast milk concentrations data.>>“The mean total BPA urinary concentration among the exclusively formula-fed infants (13.1 μg/L) was lower than those exclusively fed breast milk (23.3 μg/L), a difference that did not reach statistical significance.”<<not statistically significant given that they had deleted the two highest readings>>  “Breast milk and formula samples did not differ in total BPA concentration.” (!) (Duty et al., Potential Sources of Bisphenol A in the Neonatal Intensive Care Unit, Pediatrics. 2013 Mar; 131(3): 483–489. doi:  10.1542/peds.2012-1380, PMCID: PMC3581842  at



Appendix B:  Increased transfer, absorption and accumulation of mercury linked with type of infant feeding:


1) Transfer of mercury according to type of feeding:

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

-- According to researchers contracted by the EPA, "a wealth of information" indicates that lactational transfer of maternal mercury during the first 15 days of lactation is equal to about a third of the total transfer of mercury that takes place during gestation.  (Exploration of Perinatal Pharmacokinetic Issues  Contract No. 68-C-99-238, Task Order No. 13  Prepared for EPA by: Versar, Inc. EPA/630/R-01/004, Section,  at  )

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

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

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

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

-- Another study found over-200% increases in infant mercury levels due to 6 months of breastfeeding. (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 the Taiwanese study (Chien et al., above) that over 95% of an infant’s exposure to mercury was from breastfeeding, the increase in the infants’ mercury levels attributable to breastfeeding was probably well over 200% during the first 6 months of breastfeeding.


2) Absorption and accumulation of mercury according to type of infant feeding:

A study with infant monkeys found that their mercury concentrations showed a sudden drop after switching them from milk to solid foods; that was accompanied by a sharp increase in fecal mercury excretion. (Lok, E. 1983. The effect of weaning on blood, hair, fecal and urinary mercury after chronic ingestion of methylmercuric chloride by infant monkeys. Toxicology Letters, Volume 15, Issues 2–3, February 1983, Pages 147–152, abstract at  In that study’s charts below, observe the sharp drop in concentrations occurring after weaning, along with the concurrent increase in excretion.)

Fig. 6

Milk might promote gut absorption of ingested methylmercury, or solid food might promote flow of intestinal content containing or binding to mercury, or both.  In any case, judging by this experiment with near relatives of homo sapiens, milk feeding vs. solid foods apparently makes the difference between a growing accumulation of methylmercury in the infant body and buildup-avoiding excretion of this toxin.  Also, according to the ATSDR, infants’ absorption of metals “is generally high when they are on a milk diet.”(20e) 


One may have thought that increases in breastfeeding would have led to proportionate declines in feeding of non-human milk, but that was apparently not the case.  Most of what the increased breastfeeding was replacing was feeding of foods other than milk or formula.  In 1980, as of two months of age, over half of U.S. infants were fed infant cereal, not to mention feeding of other baby foods; but that had declined to 20% by 1991, indicating a major decline in feeding of solid foods to infants during the 1980’s and 1990’s. (Fomon, Infant Feeding in the 20th Century: Formula and Beikost, J. Nutr. February 1, 2001 vol. 131 no. 2 409S-420S, Figure 10  at  Even though breastfeeding replaced formula feeding considerably during the early months after birth, formula feeding came to be a continuation of infant feeding much farther into the first year after birth than had been the case in earlier years.  At nine months of age, the total of formula feeding plus formula-combined-with-breastfeeding in 1991 was more than twice what it had been in 1981; and it quadrupled between 1980 and 1998, to about 85%. (Fomon, Fig. 8) 

To summarize:  Feeding of non-milk foods to infants declined dramatically during the 1980’s and ‘90’s. (Fomon, 2001, Fig. 10).  And it is very likely that feeding of non-milk foods to infants has continued to decline since then, especially since breastfeeding rates have continued to increase since then.   Bearing this in mind, remember from above the ATSDR statement about infants’ absorption of metals being high when they are on a milk diet, and the chart above showing accumulation of mercury stopping after a milk diet ends.



Appendix C:  Lead effects, and some exposure declining while other exposure increases:

Lead is most commonly known for adverse effects on cognitive abilities, specifically IQ; but its effects are much wider than that.  Lead’s effects encompass essentially all of the neurodevelopmental and mental health disabilities that were measured in the Houtrow et al. study.  (Details to follow)  First, note the specific conditions that parents were asked about, which the Houtrow study found to be generally increasing:  whether their child “received special education services,… had difficulty with memory or had any other limitation… a vision or hearing problem… intellectual deficit or mental retardation; emotional or behavior problems; epilepsy; learning disability; speech problems; attention-deficit/hyperactivity disorder… or other developmental problem.”(21a)


Then note how well effects of lead, as found in many studies cited by several authoritative agencies, match with the above deficits of concern:

According to the National Research Council of the National Academy of Sciences, lead exposure has been associated with behavioral and motor  coordination problems,  shorter attention span, far more receiving speech therapy, poor school performance (even though reduction in IQ was only minor, school performance was poor mainly because of behavior problems), seizures, frequent temper tantrums, verbal and perceptual problems.(21b)  The U.S. ATSDR cites many studies in support of its statement about “reported neurobehavioral deficits in children associated with PbBs” (lead blood levels) at a certain level, and “an apparent lack of threshold down to even the lowest PbBs recorded in these studies,” (21e) as well as ADHD and hearing impairment.(21g)  A publication of WHO refers to effects of low-level exposure to lead as “irritability, hyperactivity, aggression and seizures …, impairment of the auditory brain…, impaired attention.(21f)    A team of 15 scientists found that “perceptual-motor skills” are especially sensitive to lead exposure.(21c) (Consider how well perceptual abilities would relate to the “vision or hearing” problems considered in the Houtrow study.)  “Neurodevelopmental” and especially “Neurobehavioral” disorders and attention problems are stated as being associated even with “low” or “very low” lead levels in numerous studies.(21d)  A publication of the EPA lists many of these same effects of lead exposure in young children, effects that extend well beyond the well-known cognitive effects.(21h)


It is safe to say on the basis of the above that the conditions known to be greatly increased in children by lead exposure are very similar to the neurodevelopmental disorders and mental effects found in the Houtrow et al. study to be increasing dramatically in recent years.  So the general declines in lead levels in children in recent years would have been working in the direction opposite to the direction of the recent increases in disabilities. 


When breastfeeding is extended, there is special relevance in the following statement from a publication of the National Research Council of the National Academy of Sciences:  “a diet containing lipids or milk increases absorption of lead;  this publication described results of an experiment in which rat pups continuing on a milk diet absorbed 9 to 20 times the percentage of lead compared with control rats that had been weaned.(20c)


Continuing lead exposure of many infants:

Although lead has generally been declining in the environment in recent decades, there are still many children with exposure to hazardous levels of that metal:  According to the CDC, as reported by the ATSDR, “the most common source of lead exposure for children is lead-based paint that has deteriorated into paint chips and lead dusts.” (ATSDR report, “Lead,” Ch. 6, at, p. 363)  A study in Canada found that women who resided in homes that were over 30 years old or had drunk three or more cups of coffee in the preceding 24 hours had higher lead levels in their breast milk. (p. 371 of above)   Also according to the ATSDR, exposures have been identified in lead workers' families in nearly 30 different industries and occupations, with infant exposures being a result.  Children of occupationally-exposed workers were found to have 5 to 20 times the likelihood of high blood lead levels compared with children in the general population.  Household hobbies and artistic activities of adults can also expose children to lead, including stained glass, pottery, painting and screenprinting. (p. 373 of above)


So there are clearly still many infants with hazardous exposures to lead, especially considering that no safe level of lead has been found.  Given that, we should think carefully about the advisability of the major increase in recent decades in duration of predominantly-milk feeding of infants, given the National Academy of Sciences’ reference to milk-fed animals’ absorbing 9 to 20 times the percentage of lead compared with animals that had been weaned.(20c)  A similar concern should also apply to mercury exposure.



Appendix D:  More on effects of PBDEs, and about reporting that overlooks adverse effects of postnatal exposures:


A 2011 California study of effects of PBDEs provides another example of the apparently widespread practice of scientists’ reporting results in a way that conforms with prevailing beliefs, while sometimes misrepresenting the observed data.  That study (Hertz-Picciotto et al., 2011)61  made observations of associations between developmental delay and ASD, on one hand, and child levels of PBDEs on the other.  Since the data related to developmental delay is of particular interest here, some explanation of that classification is in order.  Although the term “developmental delay” implies optimism about eventual normalcy, the odds of a favorable outcome are apparently not good. That term is sometimes used by mental health professionals interchangeably with “mental retardation,” with both categories having similar criteria; developmental delay is normally reserved for younger children, “whereas the term mental retardation is usually applied to older children when IQ testing is more valid and reliable.”63  In the only readily-found study relating the two classifications numerically, 60 percent of preschoolers with developmental delay met criteria for mental retardation.62  In what appears to be the only study that has assessed adult outcomes of children who had developmental delays, minimal hope was provided that the child’s developmental status would ever improve past the stage of mental impairment.64  In 2009-2010, about as many U.S. children age 3 to 21 were classified as developmentally delayed as were diagnosed with autism, even though the classification of developmental delay is normally applied only to children up to age 9; so there were as many children born over a period of only six years who had developmental delay as were born over an 18-year period who had autism.  And children with that seriously adverse diagnosis have been increasing rapidly in the 2000’s, with an 88% increase between 2000-2001 and 2012-2013.65  But, unlike the case of ASD, there appears to be nobody authoritatively challenging the reality of the increases in developmental delay.66  The 88% increase meant that 189,000 more American children were reported to be within this seriously negative classification in 2012-2013 than in 2000-2001, while increases in all disabilities combined were only 2 percent.65


Given the seriousness of developmental delay, its prevalence, and its rapid recent increases, it is especially surprising when a study headed by a highly-published scientist almost ignores evidence of substantial associations between this condition and child exposures to a recognized toxin.  Observe the data, which is located rather inconspicuously in a Supplemental Table of the study, accessible only by downloading a separate file. (see below) 


(The various BDEs are variations of PBDEs)

Notice the relationships between concentrations of lower-brominated PBDEs in developmentally-delayed (DD) children and concentrations in typically developing (TD) children, in the average figures marked in red below the middle of the chart.  The developmentally-delayed group had 56%-higher average levels of these PBDEs than the normal children; and levels of all eight members of the lower-brominated range of PBDEs were individually higher in the developmentally-delayed group compared with the equivalent levels in the typically-developing group. (see all entries directly above each of the red rectangles)


At very low levels of exposure, the PBDEs would not be expected to have a significant effect or to lead to a significant difference between the impaired group and the normal group; and in fact there was no difference  at that lowest measured level (5th percentile).  However, at every measured percentile level above the 5th percentile, there was a large difference between the two groups in average PBDE concentrations; concentrations were 126% higher in the impaired group than in the normal group at the 95th percentile (1635.46 compared with 723.31).  These differences in PBDE levels between the two groups (and lack of difference at the bottom) were consistent with possible effects of PBDEs on neurological development.   


So it might seem puzzling that the authors of this study stated that children with developmental delay “were similar to typically developing controls for all PBDE congeners” and that the study’s findings were “null.”  The authors provided a chart (at showing some of the above data on a log scale, in which each increment changes by a factor of 10 as part of a log scale,67 with the result that the differences cited just above appeared 10 times smaller than they would appear on a normal scale.  A seemingly-small 5% difference in the chart as shown actually represents a 50% difference in PBDE concentration.  To become aware of the real meaning of what is shown in that chart, the reader must (a) first read the words “log pmol/g lipids” turned perpendicular on the far left side of the chart, and also (b) be aware of and alert to the fact that a log scale can make large actual differences appear to be insignificant, on a chart.  There are no numbers shown that provide clues as to the major change in the scale with each increment, such as 0 -10 -100 -1000, as would typically appear on a log scale.  The authors seemed to have no interest in enabling the general reader to notice the magnitude of the actual differences that are detectable in their data.  On the other hand, they used plentiful plain language to repeatedly express their contention that the differences found were “minimal” (said twice) and to state that the study’s findings were “null” (said three times).  Remember that these “null results” indicated, upon close examination, an average of 56%-higher PBDE concentrations among developmentally-delayed children compared with typically-developing children; they also showed higher PBDE levels in all eight of the individual lower-brominated BDE congeners among the developmentally delayed group.  And at all four measurement totals by percentile level above the lowest level, PBDE concentrations were substantially higher among the developmentally delayed than among normal children.  Despite all of the above consistent and large differences between the impaired group and the controls, the authors repeatedly alleged that their findings were null.


The above study and the one in Introduction Part 1 are two easily-found examples of reported findings’ significantly conflicting with the actual data in the studies.  The authors who are doing this kind of reporting, shaping (or mis-shaping) general beliefs about children’s vulnerability to toxins postnatally, are not novices or lacking in influence.  Author searches on Pubmed brought up 250 studies of which Hertz-Picciotto is an author (principal or contributing) and 50 studies of which P.W. Davidson is an author.


Again, as was seen to be the case in the Davidson et al. study in Introduction Part 1, there seems to be a tendency for research findings to be reported that unjustifiably conform to the prevailing view to the effect that postnatal toxic exposures do not have significant harmful effects.  One unusual characteristic of these two studies was that data was provided that made it possible (with some critical examination) to get a more accurate picture than was reported in the summaries and in the text.  In most studies, the potentially contradictory data would not be provided.  In a great many cases, all the reader sees is data that the authors say has been “adjusted,” with adjustments as determined by the authors, with no explanation of how the adjustments were arrived at.  There is clearly ample freedom for authors to produce and publish reports that conform to general expectations, regardless of whether those reports as published are compatible with the actual data.



Appendix E:  Major increase in exclusiveness of breastfeeding at the turn of the century:

As indicated in Figure 2 above, U.S. breastfeeding rates as of 1998 were still the same as they had been in 1982.  In addition to the percentage increases in breastfeeding that were taking place as of 1999, the intensity of breastfeeding began to increase not long after that, in ways that are not obvious from the lines on the chart, as will be explained.


Shortly before the turn of the century, as of the mid-1990’s, the attitudes of most U.S. pediatricians were “less than positive” about breastfeeding, as found in a 1995 survey conducted for the American Academy of Pediatrics. (Schanler et al., Pediatricians’ Practices and Attitudes Regarding Breastfeeding Promotion, Pediatrics,  Vol. 103 No. 3 March 1999,  at  In response to the statement, “Breastfeeding and formula-feeding are equally acceptable methods for feeding infants,” 93 pediatricians indicated that they agreed, compared with only 72 who disagreed. The authors also noted that “The Survey reflects the opinions of respondents who were sufficiently interested in breastfeeding to complete the questionnaire. (29% did not respond to the survey.) Thus, even in this population of “interested” respondents,… their less than positive attitude is noteworthy.”)   But within less than a decade after that, exclusive breastfeeding became widely recommended by doctors, bringing a major increase in the intensity of breastfeeding.  In a study published in early 2001, the authors stated that a consensus has emerged among health professionals that exclusive breastfeeding for ~6 months should be universally recommended as the best strategy for infant nutrition and health.”( Wright and Schanler, The Resurgence of Breastfeeding at the End of the Second Millennium, J. Nutr. February 1, 2001 vol. 131 no. 2 421S-425S  at

 Fig. 7

The increase in intensity of breastfeeding after the turn of the century was accompanied by rapid increases in both percentages and durations of breastfeeding that were also taking place during those years. (see this chart)


So there is good reason to see the increase in effective breastfeeding exposure after 1998 as being even steeper than the percentage increases indicated by the upper two lines on the Surgeon General’s chart. 




Appendix F:  Apparently favorable effects of mercury on girls may not be actually favorable:

Mercury is a known endocrine (hormone) disruptor, one of the type of chemicals that is known to affect child development.(i)  One of its effects may be to accelerate development of females; in a study of a population that had high mercury levels due to seafood consumption, earlier reaching of milestones by infants (not distinguished by gender) was found to be associated with higher mercury levels in those infants;(j) this rapid development should be seen in combination with the Davidson et al. study and others (see Fig. 1 above and following text) indicating comparatively favorable effects of mercury on girls.   Such an effect, bringing rapid maturing of the brain and therefore higher student test scores, may seem benign at first; but other outcomes of faster development are likely to include the increasingly prevalent early puberty, the greater breast cancer risk that is linked with early puberty, and premature aging.(k)  Dogs and many other animals mature more rapidly than humans, and along with that goes a shorter lifespan.



Appendix G:   Additional evidence of contrasting harmful effects of environmental toxins, especially mercury and pesticides, on males versus females:


--  In a large 2013 study of autism incidence in relation to perinatal exposures to atmospheric toxins in the U.S. (Roberts et al.), it was found that risk of having autism was associated with top-quintile exposures to atmospheric metals, especially mercury and nickel, but in opposite directions for boys versus girls; the odds ratios for those two metals in relation to autism were 1.6 and 1.9 for boys, compared with 0.5 and 0.7 for girls. (1.0 is no risk.) (d)  That moderately-increased odds ratio for effect of atmospheric mercury on boys should be seen in light of the fact that inhalation appears to normally be only a very minor source of infant mercury exposure, compared with the predominant source; in what was apparently the only study that has researched such numbers, exposure to mercury via inhalation was found to be less than 4% of normal total infant exposure.(e)  

  -- A 2014 study of children with mercury levels “typical of the U.S. fish-eating population,” by a seven scientist team (Orenstein et al.), found that the negative association between methylmercury and the Learning Index was far stronger among boys than among girls (β = –4.1 for boys vs. β = –0.7 for girls).(f)

  -- The authors of the study just above pointed out three other studies that also found increased sensitivity of boys, specifically, to methylmercury.(f)  

   -- A 2011 review article cited two animal studies indicating that effects of mercury exposure are worsened by testosterone, and it cited three studies finding that estrogen has protective effects against mercury.(g)  

  -- A 2010 animal study found social impairment to result in males, but not in females, following exposure to low concentrations of mercury in water; the authors noted that social impairment and disproportionate deficits in males are both basic characteristics of autism.(h)



 --  A neurobehavioral finding that has been replicated in more than one lab is an improvement in female performance and a decrement in male performance on the radial arm maze (RAM) following direct dosing of pups with the pesticide chlorpyrifos.(h2)

--  As reported in that same source, a study with mice (Belloni et al. (2011) found that treatment of the mother with the herbicide Atrazine resulted in different effects in offspring related to social interaction and cognitive performance, between males and females.

--  A study published in 2015, by a team of eight scientists, found that pyrethroid pesticides were associated with ADHD diagnosis and symptoms in boys but not girls.(h3)


 --  In a 2014 study of effects of developmental exposure of mice to organochlorine pesticides, it was found that there was damage specifically in the frontal cortexes of male offspring, damage of a kind that “may underlie the neurobehavioral deficits observed following developmental exposure to endosulfan and other organochlorine insecticides.” (Wilson et al., Developmental exposure to the organochlorine insecticide endosulfan alters expression of proteins associated with neurotransmission in the frontal cortex, Synapse, 2014 Nov;68(11):485-97. doi: 10.1002/syn.21764. Epub 2014 Jul

    A parallel study stated that “these findings suggest that development during gestation and lactation represents a critical window of susceptibility to endosulfan exposure,” again with reference specifically to effects on males. (Wilson et al., Developmental exposure to the organochlorine insecticide endosulfan damages the nigrostriatal dopamine system in male offspring, Neurotoxicology, 2014  at


 -- A 2015 study by a different scientist also found harmful effects of exposure to endosulfan during neurodevelopment, “with significant alterations to select synaptic proteins” in the frontal cortex, in males specifically. The author considered this to be especially significant in that “a diversity of neurological deficits have their root in pathology associated with the frontal cortex.” (Caudle, Vulnerability of synapses in the frontal cortex of mice developmentally exposed to an insecticide: Potential contribution to neuropsychiatric disease, Neurotransmitter (Houst) 2015, NIHMSID: NIHMS689545  at


 -- Although boys appear to generally be more sensitive to pesticides’ effects than girls, that is not always the case.  A 2013 study reported that “in girls, total difficulties were 4.92 more likely when doubling cord blood p,p'-DDE,(an organochlorine pesticide and breakdown product) whereas no significant association was found in boys.” (Sioen et al., Prenatal exposure to environmental contaminants and behavioural problems at age 7-8years, Environ Int., 2013, Epub 2013 Jul 9. at


-- Another study dealing with effects of pesticides on males vs. females is found not far below in the section, Biological rationales…”



 -- In a document produced by the U.S. Institute of Medicine and published by the National Academies Press, the following was reported as of 2004:  In the population aged 21 to 64, females with cognitive disabilities slightly outnumbered males with such disabilities, whereas among 5-to-15-year-old children, there were almost twice as many males with cognitive disabilities as females.  Among 16-to-20-year olds, the ratio was between those two extremes.(h1)  This suggests that a transition has been occurring over recent decades, from approximate gender equality in cognitive disabilities to a far higher percentage of males with such impairments.  Such a rapid transition could not possibly be due to genetic changes, and therefore is probably resulting from changes in exposures to toxins that affect the two sexes differently.


Quoting directly from a good article dealing with this topic, In a recent epidemiologic study examining the impact of prenatal exposure to phthalates, common plasticizers, on reproductive development, adverse effects were only observed in male children (Swan, et al., 2005). Conversely, in a study examining the impact of bisphenol A (BPA) exposure on behavior in children, effects were observed especially among female children (Braun, et al., 2011). Notably, many studies of the adverse effects of endocrine disrupting compounds on cognition and behavior do not investigate differential effects in males vs. females (Engel, et al., 2009; Whyatt, et al., 2012). In general, the evaluation of child sex as a potential effect modifier of the effects of environmental toxicants on child development has received little attention in epidemiologic studies to date (Schwartz, 2003; Vahter, et al., 2007; Vahter, et al., 2007).” (Horton et al., Does the home environment and the sex of the child modify the adverse effects of prenatal exposure to chlorpyrifos on child working memory?  Neurotoxicol Teratol. 2012 Sep-Oct; 34(5): 534–541. Published online 2012 Jul 21. doi:  10.1016/ PMCID: PMC3901426 NIHMSID: NIHMS504636, at


Biological rationale for the above:

Continuing from the same (Horton et al.) article just cited, “Several factors may contribute to the differential vulnerability to CPF (chlorpyrifos pesticide) by sex. One potential explanation is CPF’s role as an endocrine disrupter. CPF has been shown to have anti-androgenic effects reducing serum testosterone levels in rats (Kang, et al., 2004)…. Males have a slower rate of cortical development than females, making the male brain susceptible to insult for a longer period (Taylor, 1969).”




 a) The accuracy of the statements regarding autism and ADHD are well known.  For learning disabilities, see entries for

--“limitations” and “inability” regarding major activities (which are the categories within which learning disabilities would have been included at that time) for 1963 and 1969-1970 in the CDC’s Data from the National Health Survey charts at, Table 1 and, Table B, and

-- learning disabilities in Table 3 of CDC’s Summary Health Statistics for U.S. Children: National Health Interview Survey, 1997 at  and

-- learning disabilities in Table 3 of CDC’s Summary Health Statistics for U.S. Children:  National Health Interview Survey, 2012, at

     Very uneven ratios in mental retardation can be seen in various sources, including Van Naarden Braun et al., Trends in the Prevalence of Autism Spectrum Disorder, Cerebral Palsy, Hearing Loss, Intellectual Disability, and Vision Impairment, Metropolitan Atlanta, 1991–2010, PLoS One. 2015; 10(4): e0124120, Published online 2015 Apr 29. doi:  10.1371/journal.pone.0124120 at  and also

Maulik et al.,Epidemiology of Intellectual Disability, at


a1)  Boyle et al., Trends in the Prevalence of Developmental Disabilities in US Children, 1997–2008, Pediatrics, Volume 127, Number 6, June 2011, at


b)  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


c) This statement based on (a) public statements by scientists expressing such a view (see Section 5.a at, (b) a January 24, 2014 e-mail received from Alycia Halladay, PhD, senior director of environmental and clinical sciences for Autism Speaks, and (c) an August 7, 2014 e-mail form Dr. Martha Herbert, MD, PhD.  The same general position is evident in the many studies that assess levels of a mother’s toxins or exposures at approximate time of birth (often as found in breast milk) and that consider the significance of those levels to relate only to prenatal exposures, when associating them with outcomes later found in the child.


c1) For a good summary of many types of reporting bias, see Table 2 of "AHRQ Series Paper 5: Grading the strength of a body of evidence when comparing medical interventions."


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


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


f) Orenstein et al., Prenatal Organochlorine and Methylmercury Exposure and Memory and Learning in School-Age Children in Communities Near the New Bedford Harbor Superfund Site, Massachusetts, Environ Health Perspect. 2014 Nov; 122(11): 1253–1259. Published online 2014 Aug 6. doi:  10.1289/ehp.1307804  PMCID: PMC4216164  at


g)  Garrecht et al., The plausibility of a role for mercury in the etiology of autism: a cellular perspective, Toxicol Environ Chem. 2011 May-Jul; 93(5-6): 1251–1273. Published online 2011 May 20. doi:  10.1080/02772248.2011.580588

PMCID: PMC3173748 at


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


h1)  Institute of Medicine, Committee on Disability in America, 3. Disability Trends:  The Future of Disability in America, Field and Jette editors, Table 3-1, National Academies Press (US): 2007


h2) Burns, Pesticide Exposure and Neurodevelopmental Outcomes: Review of the Epidemiologic and Animal Studies, J Toxicol Environ Health B Crit Rev. 2013 Apr; 16(3-4): 127–283. PMCID: PMC3705499  at

One of the studies referred to here may have been:  Levin and 6 others, Persistent behavioral consequences of neonatal chlorpyrifos exposure in rats, Brain Res Dev Brain Res. 2001 Sep 23;130(1):83-9. at


h3) Wagner-Schuman and seven others, Association of pyrethroid pesticide exposure with attention-deficit/hyperactivity disorder in a nationally representative sample of U.S. children, Environ Health, 2015 May 28;14:44. doi: 10.1186/s12940-015-0030-y.  at


i)  WHO:  State of the Science of Endocrine Disrupting Chemicals -- 2012, p. xii, accessible as "the full report" at WHO web page at  Noting that studies of wildlife provide important information about effects of toxins, this publication states that “data showing effects on growth, development and behaviour in wildlife exist for some PCBs and mercury.”


j)  Grandjean et al., Milestone development in infants exposed to methylmercury from human milk, Neurotoxicology, 1995 Spring;16(1):27-33. at


k)  According to an author/doctor (Joel Fuhrman) who has devoted considerable study to the subject, “Early puberty is an early sign of premature aging,” at





1) Houtrow et al., Changing Trends of Childhood Disability, 2001–2011, Pediatrics Vol. 134 No. 3 September 1, 2014 at   Address correspondence to Amy J. Houtrow, MD, PhD, MPH, 4401 Penn Ave, Pittsburgh, PA 15224. E-mail:


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


2a) B. Weiss and P. Landrigan, The Developing Brain and the Environment: An IntroductionEnvironmental Health Perspectives * Vol 108, Supplement 3 * June 2000  at

“…we know the causes of fewer than 25% of neurodevelopmental disabilities.”


3) Collaborative on Health and the Environment’s Learning and Developmental Disabilities Initiative, Scientific Consensus Statement on Environmental Agents Associated with Neurodevelopmental Disorders, at 


4) at


5) Population counts for those age groups in those years do not appear to be available, but total birth numbers are available for the relevant birth years, indicating a 7% increase from the birth years of the earlier group to those of the later group.


7)  Boyle et al., Trends in the Prevalence of Developmental Disabilities in US Children, 1997-2008, Pediatrics, May, 2011, at

8)  CDC statement, commenting on Boyle et al study:   “Data from the study showed that developmental disabilities (DDs) are common: about 1 in 6 children in the U.S. had a DD in 2006–2008. These data also showed that prevalence of parent-reported DDs has increased 17.1% from 1997 to 2008. “      CDC:  Key Findings: Trends in the Prevalence of Developmental Disabilities in U. S. Children, 1997–2008, at

9) CDC, Vital and Health Statistics, July 2008, Diagnosed Attention Deficit Hyperactivity Disorder and Learning Disability: United States, 2004–2006  at, p. 7

10)  Grandjean and Jensen, Breastfeeding and the Weanling’s Dilemma   Am J Public Health. 2004 July; 94(7): 1075.   PMCID: PMC1448391 at

11)  Re: EPA’s RfD for dioxin:   At  in section 4.3.5, at end of that section, "...the resulting RfD in standard units is 7 × 10−10 mg/kg-day."  (that is, O.7 pg TEQ/kg-d)  

Re: breastfed infants’ exposures to dioxins, in U.S. and internationally:

- Infant Exposure to Dioxin-like Compounds in Breast Milk  Lorber (Senior Scientist at EPA) et al., VOL. 110  No. 6  June 2002,  Environmental Health Perspectives

- 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.

-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

- 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

- 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

- 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

- 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

- J Grigg,  Environmental toxins; their impact on children’s health, Arch Dis Child 2004;89:244-250 doi:10.1136/adc.2002.022202 at


 12)  Re:  PBDEs ingested by breastfed infants:

-Table 5-4 of EPA  (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F., Schechter (2006) study in first page of table.(daily dose of 306 ng/kg-d for breastfed infants)    Also Section 5.6.2, near end of section, of above.

- Costa et al., Developmental Neurotoxicity Of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Neurotoxicology. 2007 November; 28(6): 1047–1067. PMCID: PMC2118052  NIHMSID:

- EPA Technical Fact Sheet on Polybrominitated Diphenyl Eithers (PBDEs) and PBBs, p.4   at --  RfDs: 1 x 10-4 mg/kg/day (=100ng/kg/day)  for the BDE 47 and 99 congeners. (Note that BDE 47 typically constitutes over half of the PBDEs present in humans.  --  Daniels et al., Individual Characteristics Associated with PBDE Levels in U.S. Human Milk Samples, Environmental Health Perspectives, at Regarding prevalence of tetraBDEs (47), see also Costa LG, et al., Polybrominated diphenyl ether (PBDE) flame retardants: environmental contamination, human body burden and potential adverse health effects. Acta Biomed. 2008 Dec;79(3):172-83  at

13) Re:  Mercury levels in breast milk:

- U.S. ATSDR document on mercury at, p. 443

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

14)  Re:  PCBs in human milk:  U.S. Agency for Toxic Substances and Disease Registry, Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000,  at   This ATSDR report quotes a range of concentrations of PCBs in human milk as from 238 to 271 ng/g lipid weight. 1 g lipid weight = about 25g whole weight (assuming 4% fat in human milk).  So the concentrations found in the studies were about 250 ng/25g whole weight, which = 10ng/g whole weight.  1 g (gram) = 1 ml of water., so the 10 ng/g whole weight is the same as  10ng/ml.  That is the same as 10,000 ng per liter, which is the same as .01 mg/liter.  So the levels of PCBs in human milk seem to be about .01 mg/liter, compared with .0005 mg/liter, the maximum allowed by law in U.S. public water systems.  That is, about 20 times the concentration that would be allowed in public water systems. (U.S.EPA, Drinking Water Contaminants, National Primary Drinking Water Regulations, at  

15)  Re: dioxins in formula less than 1% of dioxins in breast milk:

- U.K. Food Standards Agency Food Survey Information Sheet 49/04 MARCH 2004, Dioxins and Dioxin-Like PCBs in Infant Formulae,  found at

- 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

 Re:  PBDEs in formula less than 2% of concentration in breast milk:

-Section 4.7 , 2nd paragraph (citing Schechter et al.) of U.S. EPA  (2010) An exposure assessment of polybrominated diphenyl ethers.  http:/

-Section 5.6.2 of above, 2nd paragraph.  The EPA states the figure as "44.1 ng/g lwt"  (44.1 ng = 44,100 pg).  For comparison purposes, the lipid (fat) weight indicated here needs to be converted to whole weight, which can be done as follows:  The EPA here assumes a fat content of 4%.  Using that figure, 44,100 pg/g lwt becomes 1760 pg/g wwt.

 Re:  Mercury in formula less than 1% as high as in human milk:

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

-Re:  PCBs in infant formula typically less than 1% but up to about 4% as high as in human milk:

-  In breast milk:  About 250 ng/g lipid weight.  In soy-based formula:  about 10 ng/g lipid weight.  U.S. Agency for Toxic Substances and Disease Registry, Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000, pp. 560, 573, at  Data does not appear to be available for PCBs in cow’s-milk-based infant formula, but data for whole milk could give an approximation, as follows:  adding together the figures for the two kinds of PCBs in the following study provides a range of  52 to 2455 ng/kg fat, which equals .05 to 2.45 ng/g fat (lipid)  (Krokos et al., Levels of selected ortho and non-ortho polychlorinated biphenyls in UK retail milk, Chemosphere. 1996 Feb;32(4):667-73.  at 

15a) WHO:  State of the Science of Endocrine Disrupting Chemicals -- 2012, p. 119, accessible as "the full report" at WHO web page at

16) "Surgeon General's Call to Action to Support Breastfeeding, 2011," p. 6 and Fig. 1,  at

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

19) The CDC’s home page for this historical breastfeeding data is at

20) Exhibit 3-2 of National Longitudinal Transition Study 2:  Youth with Disabilities:  A Changing Population,  Prepared for:  Office of Special Education Programs, U.S. Department of Education at  5.2 percentage point increase divided by 8.4= 62% increase, etc.; averaging the data for the three educational levels below college graduate shows a 6% decline in their disabilities while their percentage of the population declined 9%

20a1) WHO, 622.Lead (Food Additives Series 21), Evaluation of Health Risk to Infants and Children, at

20b) Li et al., Transfer of lead via placenta and breast milk in human, Biomed Environ Sci. 2000 Jun,

20c)  National Academy of Sciences, National Research Council, 1976: Recommendations for the Prevention of Lead Poisoning in Children, at

20d)  EPA lead document at, p. 4-7;  Castellino et al., Inorganic Lead Exposure and Intoxications, CRC Press, at; p. 134.

20e) U.S. ATSDR, Lead, Ch. 6, at,  p. 372

20f) Mason et al., Pb Neurotoxicity:  Neuropsychological effects of Lead Toxicity, Bio Research International, 2014, at

21) CDC charts accessible at

21a) Childhood disability rate jumps 16% over past decade, in AAP news (of American Academy of Pediatrics), at

21b) National Academy of Sciences, National Research Council, 1976: Recommendations for the Prevention of Lead Poisoning in Children, at

21c) Wasserman (and 14 other scientists): Lead exposure and intelligence in 7-year-old children: the Yugoslavia Prospective Study, Environ Health Perspect. Sep 1997; 105(9): 956–962., PMCID: PMC1470353

21d)  Chiodo et al., Neurodevelopmental effects of postnatal lead exposure at very low levels, Neurotoxicol Teratol. 2004 May-Jun;26(3):359-71. The results consistently show neurobehavioral deficits in relation to low levels of lead in the areas of intelligence, reaction time, visual-motor integration, fine motor skills, attention, including executive function, off-task behaviors, and teacher-reported withdrawn behaviors. Effects were identified in the specific domains of attention, executive function, visual-motor integration, social behavior, and motor skills, which have been previously suggested as part of lead's "behavioral signature"

Winneke et al., Neurobehavioral and neurophysiological observations in six year old children with low lead levels in East and West Germany, Neurotoxicology. 1994 Fall;15(3):705-13.

Walkowiak, Cognitive and sensorimotor functions in 6-year-old children in relation to lead and mercury levels: adjustment for intelligence and contrast sensitivity in computerized testing, Neurotoxicol Teratol. 1998 Sep-Oct;20(5):511-21.  <<attention>

Winneke et al., Neurobehavioral aspects of lead neurotoxicity in children, Cent Eur J Public Health. 1997 Jun;5(2):65-9.

Dietrich et al., Lead exposure and the motor developmental status of urban six-year-old children in the Cincinnati Prospective Study, Pediatrics. 1993 Feb;91(2):301-7.

Tellez-Rojo et al., Longitudinal associations between blood lead concentrations lower than 10 microg/dL and neurobehavioral development in environmentally exposed children in Mexico City, Pediatrics. 2006 Aug;118(2):e323-30.

Bellinger, Very low lead exposures and children's neurodevelopment, Curr Opin Pediatr. 2008 Apr;20(2):172-7. doi: 10.1097/MOP.0b013e3282f4f97b.

Calderon et al., Exposure to Arsenic and Lead and Neuropsychological Development in Mexican Children, Environmental Research, Volume 85, Issue 2, February 2001, Pages 69–76 at

Al-Saleh et al., Relationships between blood lead concentrations, intelligence, and academic achievement of Saudi Arabian schoolgirls, International Journal of Hygiene and Environmental Health, Volume 204, Issues 2–3, 2001, Pages 165–174, at 

21e) U.S. ATSDR, Lead, at, p. 260 

21f) Inorganic and Organic Lead, 2006, International Agency for Research on Cancer (WHO) at pp 304-308 

21g) ATSDR:  Lead Toxicity:  What Are the Physiologic Effects of Lead Exposure? at

21h) EPA:  Children’s Environmental Health Facts at

21j) Krieger et al., Choosing area based socioeconomic measures to monitor social inequalities in low birth weight and childhood lead poisoning: The Public Health Disparities Geocoding Project (US), J Epidemiol Community Health 2003;57:186–199, at  The authors point out that “the magnitude of increased risk detected in our study for raised blood lead concentrations is similar to that reported in previous studies using both area based and individual level socioeconomic measures.”

21k) CDC: Preventing Lead Exposure in Young Children, at

22) An October, 1999 USDA publication, “WIC and Head Start” appears to provide the first mention of exclusively breastfeeding mothers’ receiving an enhanced food package, at

23)  see and, with many authoritative sources cited at both websites.


24) see for considerable detail on this topic.


25) see

26) Schecter et al.,  Polybrominated diphenyl ethers (PBDEs) in U.S. mothers' milk, Environ Health Perspect. 2003 Nov;111(14):1723-9. . found at

27) Sec. II.B of Brominated Flame Retardants, Third annual report to the Maine Legislature, 2007, D Rice et al., citing Li et al., 2005a

28) Herbstman et al., Developmental Exposure to Polybrominated Diphenyl Ethers and Neurodevelopment. Curr Environ Health Rep. 2014 Jun 1;1(2):101-112.  at

29) at, pp. 9-10)

30)  Flame Retardants in Furniture, Carpets Might Affect Kids' Development:  California study found that higher exposures were linked to IQ, attention deficits  HealthDay, Medline Plus, NIH  11/25/2012, at,  This article was reporting about Eskenazi B et al., In utero and childhood polybrominated diphenyl ether (PBDE) exposures and neurodevelopment in the CHAMACOS study    Environ Health Perspect. 2013 Feb;121(2):257-62. doi: 10.1289/ehp.1205597. Epub 2012 Nov 7  at


31) Costa et al., Developmental neurotoxicity of polybrominated diphenyl ether (PBDE) flame retardants. Neurotoxicol. 2007;28(6):1047–67; also McDonald, Polybrominated diphenylether levels among United States residents: daily intake and risk of harm to the developing brain and reproductive organs. Integrated Environ Assess Manage. 2005;1(4):343–54.

32) Hoffman, et al., Lactational Exposure to Polybrominated Diphenyl Ethers and Its Relation to Social and Emotional Development among Toddlers  Environ Health Perspect. 10/2012;  seeing text above Figure 3 in

33) 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

34) (Re: PBDE levels in breastfed vs formula-fed children:   Near end of Section 5.6.2 ("Impacts to Infants from Consumption of Breast Milk"), p. 5-79, of An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. online at  or directly at

35)  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   and also

 PBDEs in infant formula: Section 4.7 , p. 4-77, 2nd paragraph (citing Schechter et al.) of U.S. EPA (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment; EPA/600/R-08/086F. online at or directly at

36) Costa et al., Polybrominated diphenyl ether (PBDE) flame retardants: environmental contamination, human body burden and potential adverse health effects. Acta Biomed. 2008;79(3):172–183).

37) Counter et al., Mercury exposure in children:  a review, Toxicology and Applied Pharmacology, Volume 198, Issue 2, 15 July 2004, Pages 209–230 at

38) National Scientific Council on the Developing Child, Early exposure to toxic substances damages brain architecture, 2006),Working Paper No. 4, at

38a)  FAOSTAT Food Balance Sheets ( (Figure S4).

39) U.S. NOAA, Fishwatch: U.S. Seafood Facts, The Surprising Sources of Your Favorite Seafoods, at

40) Sloss, Mercury emissions from India and South East Asia, 2012, at

41) Trends in Blood Mercury Concentrations and Fish Consumption Among U.S. Women of Childbearing Age NHANES, 1999-2010, July 2013, Fig. 6, EPA-823-R-13-002

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

42a) Rice et al., Environmental Mercury and Its Toxic Effects, J Prev Med Public Health. 2014 Mar; 47(2): 74–83, doi: PMCID: PMC3988285  at

43) Vogel, Battles Over Bisphenol A, at, referring to "Chemical Profile: Bisphenol A," Chemical Marketing Reporter, May 26 1980, p. 9.

44)  U.S. EPA,  Bisphenol A Action Plan (CASRN 80-05-7), accessed 4/5/2015 at

45) Flint et al., Bisphenol A exposure, effects, and policy: A wildlife perspective, Journal of Environmental Management 104 (2012) 19e34, at



48) Kuwahara et al., Perinatal Exposure to Low-Dose Bisphenol A Impairs Spatial Learning and Memory in Male Rats, J Pharmacol Sci 123, 132 – 139 (2013) at ; specifics about locus coeruleus from

49) Yi et al., Association between Endocrine Disrupting Phenols in Colostrums and Maternal and Infant Health, Int J Endocrinol. 2013; 2013: 282381. Published online 2013 May 8. doi:  10.1155/2013/282381PMCID: PMC3662185  at

50) Health Canada, Archived, Survey of Bisphenol A in Canned liquid Infant Formula Products, archived on June 24 2013. at

51) When arriving at the mean figures, the data from these studies was weighted according to the number of mothers measured in each study.  Vandenberg et al., Urinary, Circulating, and Tissue Biomonitoring Studies Indicate Widespread Exposure to Bisphenol A, Environmental Health Perspectives. 2010;118(8):1055-1070  at 

Also Yi et al., Association between Endocrine Disrupting Phenols in Colostrums and Maternal and Infant Health, Int J Endocrinol. 2013; 2013: 282381. Published online 2013 May 8. doi:  10.1155/2013/282381PMCID: PMC3662185  at

52)  An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000", EPA/600/P-03/002F, November 2006: especially Table 1-17.  2000 appears to be the most recent year for which the EPA provides national dioxin release data.  The EPA data shows that, between the years 1987 and 2000 (2000 appears to be the latest year for which the EPA provides this data), dioxins released in diesel emissions increased about 100%:  a 74% increase from off-road diesel emissions (including emissions from trains, ships, construction equipment and tractors) and a 134% increase from heavy-duty diesel truck emissions during that relatively short period.

53)  Commoner et al., Center for the Biology of Natural Systems, Queens College, CUNY:  Dioxin Sources, Air Transport and Contamination in Dairy Feed Crops and Milk, 1998, at

54) 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, Figure 2, Environmental Health Perspectives • Volume 109 | Number 1 | January 2001, at

55) U.S. National Library of Medicine, Toxtown, Persistent Organic Pollutants (POPs), at

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

57)  P. Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants,  Environ. Health Perspectives, accepted Oct. 1993   Also  Marques RC, et al., Hair mercury in breast-fed infants exposed to thimerosal-preserved vaccines. Eur J Pediatr. 2007 Sep;166(9):935-41. Epub 2007 Jan 20  at   (Re: especially rapid mercury transmission in early postnatal weeks): Exploration Of Perinatal Pharmacokinetic Issues  Contract No. 68-C-99-238, Task Order No. 13  Prepared for EPA by:  Versar, Inc.  EPA/630/R-01/004   Section,  at

58) Roberts et al., "Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ Health Study II Participants," (Environ Health Perspect; DOI:10.1289/ehp.1206187 online at

See also Volk et al., Traffic Related Air Pollution, Particulate Matter, and Autism, JAMA Psychiatry. Jan 2013; 70(1): 71–77.   at

doi:  10.1001/jamapsychiatry.2013.266

See also


59)  Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. Lancet. 2006;368:2167–2178. at 

60)  Autism rates associated with nutrition and the WIC program.  Shamberger R.J., Phd, FACN, King James Medical Laboratory, Cleveland, OH  J Am Coll Nutr. 2011 Oct;30(5):348-53.  Abstract at 

61) Hertz-Picciotto et al.,,Top Polybrominated diphenyl ethers in relation to autism and developmental delay: a case-control study, Environmental Health 2011, 10:1  doi:10.1186/1476-069X-10-1, online at:


62) Crnic et al., Understanding the Emergence of Behavior Problems in Young Children With Developmental Delays; Infants and Young Children, Vol. 17, No. 3, 2004, pp. 224,226  at

63) Practice parameter: Evaluation of the child with global developmental delay, Report of the Quality Standards Subcommittee of the American Academy of Neurology and The Practice Committee of the Child Neurology Society, p. 368, at

64) Bernheimer et al., 2006, Young Children with Developmental Delays as Young Adults: Predicting Developmental and Personal–Social Outcomes, American Journal on Mental Retardation, at;2?url_ver=Z39.88-2003&;

 -- referring to children with developmental delay, the authors stated,“Developmental status at 6 to 7 was a strong predictor of developmental status in young adulthood.”  Also, according to a web page of the University of Michigan Health System, parents of children with developmental delay should have the goal ”for your child to become as independent as possible.”<>>


65) U.S. Department of Education, National Center for Education Statistics, Digest of Education Statistics, Table 204.30, Children 3 to 21 years old served under Individuals with Disabilities Education Act (IDEA), Part B, by type of disability: Selected years, 1976-77 through 2012-13 at


66)  In the case of ASD, there has been considerable publicity and increased awareness of the disorder, bringing the possibility that a very large part of the increases results from cases being noticed and diagnosed that would not have been reported in the past; the fact that about half of all children currently being diagnosed with ASD are of normal or high intelligence suggests how the disorder may have gone unreported in earlier years. By contrast with the major publicity about increase of autism, a May, 2015 Google search for “increase in developmental delay” brings up no results that fit that phrase; it yields search results about increases of other neurological disorders, but nothing about increase in developmental delay.

67) see



019) CDC, Pediatric Nutrition Surveillance, National, Table 13D, at





*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 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, while maintaining accuracy in what is said.  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(1) and

    (b) of a kind that has been authoritatively determined to be of low quality; former U.S. Surgeon General Regina Benjamin acknowledged that essentially all of the research supporting benefits of breastfeeding consists merely of observational studies.(1a)  One determination that evidence from observational studies is of low quality has been provided by Dr. Gordon Guyatt and 14 of his associates;(2) 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.(2a)  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),(2c) writing about “the disastrous inadequacy of lesser evidence,” in reference to findings from observational studies.(2b)


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 lot 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 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

Fredericksburg, VA, USA