Breastfeeding, ADHD, and Serious Child Psychological Problems


Section 1:  Origins of ADHD


Section 2:  Specific toxins linked with ADHD

Section 2.a:  Dioxins, especially long-lasting in the body

Section 2.b:  PCBs, chemically related to dioxins

Section 2.c:  PBDEs, rapidly increasing in the environment

Section 2.d:  Mercury effects

Section 2.e:  Tobacco smoke


Section 3:  What all of the above toxins have in common

Section 4:  Serious psychological problems:

Section 5:  Serious long-term outcomes related to ADHD:

Section 6:  An historical look at the rise of ADHD in the U.S. vs. in Europe

Section 7:  Testosterone:  Its importance to neurological development, and its vulnerability to developmental toxins in human milk



Section 1:  Origins of ADHD: 

ADHD (Attention Deficit Hyperactivity Disorder) was first named as a disorder by the American Psychiatric Association in 1969.1a  That provides one clue as to the approximate time of origin of significant incidence of this disorder. 


Another indication comes from a U.S. study published in 2004 which pointed out that, as of that time, it was being "increasingly recognized that attention deficit hyperactivity disorder (ADHD) persists into adulthood."(2)  So apparently a significant number of people who had recently become adults in the years leading up to 2004 were demonstrating ADHD symptoms that had not previously been observed in adults.


It is worthwhile to look back toward the neurodevelopmental origins of the young adults who would, as of 2000 to 2003, be increasingly recognized as having ADHD in adulthood.  They would have been born in the 1970’s to 1980 or thereabouts.  It is important to focus closely on the period of the infancies of those people, since infancy is the period when by far the greatest amount of neurological development takes place. (See chart below.) 1

According to widely-quoted EPA researchers (Rice and Barone), studies “have clearly demonstrated that when proliferation is actively occurring in a given region of the brain, it is vulnerable” to toxins.(2a)   This graph shows that most of the fastest growth of the brain takes place during the first year after birth.    According to the U.S. National Research Council, 83% of the human brain’s growth spurt is postnatal.(2d)   In a publication of the National Academies Press, in a section headed “Postnatal Effects of Neurotoxicants” and referring to postnatal brain development, the authors stated that toxic exposures at a particular time would differentially affect the structures undergoing peak development.(2c)   The first year of life is therefore (as shown in this chart) a period, probably the period, when neurological development is most likely to be vulnerable to effects of toxins.


Since the young people who were increasingly reaching adulthood with ADHD around 2000 to 2004 would have gone through their vulnerable infancies during the 1970’s to very early 1980’s, that is another reason to focus on that specific earlier period as the time when increasing exposure of infants to environmental toxins may have caused what was being increasingly observed in young adults 20-plus years later.  Remember also 1969 as the year when the disorder was first named.


Therefore it is worthwhile to look back a few decades to see if there may have been anything newly taking place or changing in the environment at that time that might have affected the neurological development of infants born in that period.  Experts on the subject of toxins in breast milk (Grandjean and Jensen) pointed out in 2004 that various environmental toxins "have caused contamination of human milk only during the last half century, and long-term health impacts are now being discovered."(2b)


In the middle of the 20th century, from the post-war years up until the early 1970's, breastfeeding in the U.S. was relatively rare.(3)  But breastfeeding rates started to climb in 1965 and began to increase rapidly and substantially in about 1972, as seen in the charts below.  The rates of increase were especially rapid in the 1972-1982 period.  They later continued to increase following a dip during the 1980's.

Figure 2


The above is of significance because environmental toxins that became prevalent in developed areas in the mid-20th century tend to become concentrated in human milk, as stated by the pro-breastfeeding group, MOMS (Making our Milk Safe),(4) and in considerable scientific literature.(5)  Also, remember the expert statement above about when contamination of human milk began (last half century).2b




Section 2:  Specific toxins linked with ADHD

Section 2.a:  Dioxins, especially long-lasting in the body

The EPA has determined a relatively safe threshold dose of that chemical to be 0.7 pg (picograms) of dioxin toxic equivalency (TEQ) per kg of body weight per day.(6)  In contrast with that, a research team headed by an EPA senior scientist determined in 2002 that a typical breastfed infant in developed areas ingests about 242 pg of dioxin TEQ per kg of body weight per day initially; this decreases over the period of a year of breastfeeding to less than one-tenth of that, as the mother's lifetime accumulation of that toxin is gradually excreted in the milk.(7)  That infant ingestion of dioxin is known to be scores of times higher than is ingested in infant formula.7a, 7b 


The following deals with specific apparent effects of dioxins in relation to ADHD:  

A study by an international research team (Lee et al.) found that attention deficit disorder was 202% higher among children (age 12-15) with higher levels of dioxins -- that is, over three times the risk compared with children with lower exposures.(7c)  The elevated levels of dioxins that were associated with such dramatic increase in risk of attention deficits were quite common -- found in 27% to 31% of children -- by no means exceptional exposures.  And those elevated levels of dioxins were almost certainly of early-postnatal origin, given the following:  In a 2011 study, by 13 scientists, it was determined that the median levels of dioxins in breastfed infants were doubled within 4-5 months after birth, compared with levels in formula-fed infants that were reduced by half in that same period of time; after those infants had grown to ages18 to 26, average dioxin concentrations were still twice as high in the breastfed young men as in those who had been formula fed.(7d)   In another authoritative study, the breastfed-to-formula-fed ratio of dioxin accumulation was calculated to be 6-to-1 after the first year for infants breastfed 6 months or more, and still 2-to-1 a decade later.(7e)


Therefore, since a tripled rate of ADHD has been found to be associated with higher levels of dioxins among 12-to15-year-old children, that appears to be almost the equivalent of associating greatly increased ADHD with history of breastfeeding.



Section 2.b:  PCBs: chemically related to dioxins, with some similar effects

PCBs, like dioxins, are known to be present in human milk in many-times higher concentrations than in infant formula,(8) and they have been found to be directly linked to symptoms in childhood that predict likelihood of later being diagnosed with ADHD, as will be explained.


The charts below, from a 2015 study, demonstrate substantial differences among infants in their exposures to PCBs, depending on their feeding type.  Farther down will be shown the apparent ADHD-related effects of even small differences in postnatal exposures to PCBs. 

The children in the Verner et al. study, from which these charts were taken, were breastfed for a median of less than one month (only 40% were breastfed for a month or more).8e  As seen in the charts above and on the left, the increase in PCB levels resulting from breastfeeding for less than a month would have been very minor compared with the increase that would occur after a more typical duration of breastfeeding.  And, as seen above right, the decline of PCB levels in non-breastfed infants at less than a month after birth would be small compared with the extent of the decline after several months.  However, at five months after birth (a more typical breastfeeding duration), PCB levels in breastfed infants would be over 10 times the levels in non-breastfed infants, and the difference would be rapidly increasing with each additional month of breastfeeding.  (Extremely similar results have been determined or observed in other studies.(8f)) the median duration of breastfeeding in the group studied was short, producing a relatively minor increase in PCBs; therefore it is noteworthy that statistically significant associations were nevertheless found between moderate increases in those brief, relatively low infant exposures and ADHD-related behavior at age 8.  As seen in the chart on the right, distinct effects of moderate increases in infant PCB levels during specific months of early infancy were found at age 8, even within that low-exposure group.


The authors of the Verner et al. study pointed out that the increases in ADHD-related effects associated with increases in infant exposures to PCBs were statistically significant only for exposures during a few months of infancy.  But that should have been expected, given the brevity and the relatively minor scale of the postnatal spikes in PCB levels in this specific study group.  It also appeared that the associations of ADHD-related behavior with postnatal infant exposures probably would not have occurred except for the fact that the postnatal exposures were added on top of accumulated gestational exposures; but it should be noted that the prenatal accumulations will be there for the foreseeable future, forming the base onto which the postnatal exposures would normally be added.  PCBs in the environment initially declined after they were banned from general production in the late 1970’s, but they have been stable since then and are still at hazardous levels, having been found to be present in average breast milk at 20 times the level allowed in bottled water.(8d)


The authors stated that, to the best of their knowledge, “this is the first study to assess the neurobehavioral impact of postnatal PCB exposures at low levels characteristic of contemporaneous general population samples.”  (As mentioned, the average exposures of the group studied were apparently unusually low, in major respects.)  So apparently no study has been published that indicates what the ADHD-related effects would be of a normal (much greater) exposure to PCBs via breastfeeding.  Therefore we may, for the time being, be inclined to ask some reasonable questions as to what is likely to be the case, such as follows:


Relatively minor postnatal exposure to PCBs was found to be associated with statistically significant increase in ADHD-related behaviors.


Above-average postnatal exposure to PCBs would be likely to lead to  -- ?


Unless there is reason to believe otherwise, the normal assumption is that a greater dose of a toxin would lead to greater effects.






A study of Dutch children found a strong association of exposure to PCBs specifically via breastfeeding with problems of inattention and hyperactivity in infants at 42 months after birth.(27) The study distinguished between effects of prenatal and lactational exposure and found that only the lactational exposure was associated with “less sustained attention” as well as slower reaction times. 


An experiment in which rhesus monkeys were administered very small doses of PCBs arrived at similar findings regarding hyperactivity, but also observed retarded learning ability.(14)




Section 2.c:  PBDEs:  Especially rapidly increasing in the environment

A 2011 Spanish study found that gestational exposure to PBDEs in the mothers had no significant adverse effect, but exposure to those same mothers' PBDE levels via breastfeeding did have a substantial effect, including an 80% increase in relative risk of attention-deficit problems and a 160% increased relative risk of poor social competence.(22)   It should be noted that this study was done in Europe, where PBDE levels are many times lower than in the U.S., yet the ADHD-like effects were nevertheless very measurable.


A 2012 U.S. study found that children who had consumed breast milk that was merely above the median in PBDEs were 2½ to over 3 times as likely (compared with those below median) to have high scores in activity/impulsivity behavior, of a kind that indicated likelihood of developing into Attention Deficit/Hyperactivity Disorder.(23)  


Authors of a larger 2013 study on this general topic reported that their study “largely supports” the findings of the above two studies.(24)  They found that every 10-fold increase in a child’s total PBDE level (a typical increase) was associated with 4.5 and 5.5 times higher odds of the child being rated by the teacher as being in the “moderately or markedly atypical” range on a scale of hyperactivity/impulsivity.  (Bear in mind that a child’s PBDE levels are largely determined by his or her breastfeeding history, even years later:  In the only study quoted by the EPA making such a comparison, the average total PBDE concentration in children that had been breast fed was still nearly three times as high as average concentrations in formula-fed children at age 4 (24a))


If the large possible differences in children’s PBDE levels mentioned just above sound improbable, bear in mind that various studies have found breast milk in American mothers to be 10 to 100 times higher in PBDE concentrations than the milk of European mothers.(25)  And even those much lower European levels have been a source of concern (e.g., the Spanish study mentioned above).   In 1998, research with archived samples of breast milk in Sweden found that PBDE levels in the milk had been doubling every 5 years over the preceding 25 years.(25a)


Being aware of the above-described effects of PBDEs as related to attention deficits and hyperactivity, bear in mind that EPA research has found that PBDEs are apparently more than 50 times as high in typical mother's milk as in infant formula (see Section 1.b at

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Section 2.d:  Mercury effects

Children with blood mercury levels above a certain level (elevated due to fish consumption, but still less than one-sixth of the level considered to be poisoning) were found in a Chinese study to have a 9.7 times higher risk of having ADHD, after adjustment for confounding variables.  Also, after adjusting for age, gender and parental occupational status, the mean blood mercury level was found to be 75% higher in children with ADHD (p < 0.001)25a1 


In cases of widespread accidental mercury poisoning in Iraq, the mildest cases were “characterized by hyperactivity and attention deficit.”(25a1a)


Knowing the above, note also that infants who are breastfed have been found to have two and three times the mercury levels after six months or a year of breastfeeding, compared with infants who have been bottle fed,(25a2) and also that typical human milk contains four times the level of mercury that is allowed in U.S. bottled water, and often higher.(25a3)­­


Knowing that infants’ mercury exposures vary over a full spectrum from very mild to major, and considering that moderate exposures could have significant negative effects even if they don’t result in a diagnosis of ADHD, it is relevant to see (in this chart) the apparent effects of mercury exposure in a general population of children.  Notice that, in accord with the very uneven male-female ratio of those diagnosed with ADHD, males in the general child population, also, appear to be very disproportionately affected by the adverse cognitive effects of mercury exposures. 


In line with the above, there has been a general lower level of success of males in education in relation to females in recent years; college graduation rates among U.S. females, which first rose significantly above those of males in 1996,25a5 have since then risen much more in relation to male graduation rates.  As of a 2014 publication, almost 60% of new U.S. college graduates were women, and disproportionate ratios in the same direction have also been found in most OECD countries.25a6




Section 2.e:  Effects of tobacco smoke:

According to one study, “gen­erally it appears that the children of smokers are approxi­mately 1.5–3 times more likely to have ADHD or ADHD symptoms than the children of non-smokers.(25b)  This should be seen in combination with the finding that "breast-fed infants of smoking mothers have urine cotinine levels 10-fold higher than bottle-fed infants whose mothers smoke."(25c)  (Cotinine is a marker for smoke exposure, and the mother’s absorption of products of tobacco smoke is apparently passed on to the infant via breast milk, to a large extent.)  It is entirely likely that the children of smokers who receive the greatest effects of the smoking exposure will probably be those who have the 10-times-higher cotinine evidence of smoking exposure (i.e., the breastfed ones).



Section 3:  What all of the above toxins have in common:

As indicated above, there appears to be an array of different toxins linked with ADHD.  Most infants are likely to be exposed to the first four (dioxins, PCBs, PBDEs and mercury) all at the same time (see below), or to all five at the same time if the mother is a smoker.  So it may be difficult to determine if the detected associations with one of those toxins actually results from effects of one or more of the others to which an infant is also exposed at the same time.  That is a very significant concern, if we are to attempt to reduce the exposures that are linked to ADHD.


So it is important to consider what all of those toxic exposures have in common:  their means of delivery to the developing infant.  As indicated in the earlier text, all five of them are substantially present in human milk; the first four are all present in breast milk in concentrations recognized to be well above authoritatively established safe levels,25d, 25e, 25f, 25g, and present in the main alternative feeding at levels that are a very small fraction of their concentrations in human milk.25h, 25i, 25j, 25k  


The author of this article has written to seven scientists in the field of neurological disorders (the complete science team of the major autism-advocacy organization, Autism Speaks) and asked if any of them could name any means of widespread transfer of any toxins to infants in doses recognized to exceed established safe levels, aside from the four such transfers via human milk.  As of over six months later, three responses were received, and none of those suggested that any such transfers occur by any other means.  And nobody suggested that the question was not well founded.


Given the above, as well as the evidence presented at regarding associations between these same toxins and ASD, there is reason to at least consider cutting off the major exposures to all of the above toxins at the same time by restricting consumption of human milk by infants.  But that gets to the major problem that even considering such an alternative would be opposite to the widespread belief in the medical community that breastfeeding should be recommended except in exceptional circumstances.  Considering the evidence presented above, it would seem that the medical establishment should be prepared to respond to questions about the basis for their recommendations.   However, at least three separate letters on this subject from the author of this article to the American physicians’ associations that recommend breastfeeding (AAP, AAFP, and ACOG) have brought no responses from any of them.  The American Academy of Pediatrics and the American Academy of Family Physicians both have position papers in which they cite many studies that have found benefits of breastfeeding, but they make no mention of any of the 60+ studies that have found adverse effects of breastfeeding. (see



Fig. 4

Section 4:  Serious psychological problems:

Note that the major rise of ADHD as well as serious behavioral and emotional difficulties among children apparently started only after the major rise in breastfeeding was underway.  Remember that ADHD was first named after the increase in breastfeeding had begun, and well after increases of toxins in human milk had begun, and it has apparently grown in prevalence along with the increases in breastfeeding.  And as shown in Figure 4 above, "Serious emotional or behavioral difficulties" among children was apparently first published in CDC data as of 2003, at a 5% level and increasing.  An extensive web search as well as considerable search on the CDC's website for "Serious emotional or behavioral difficulties" brings up a great deal from after the year 2000, but the only result found for earlier years was 1988 CDC data for those words but without the word "serious."  That showed 5.1% of 3-to-17-year-old children had received treatment or counseling for "emotional or behavioral problems" within the previous 12 months.(17)  That sounds very much like an intermediate step between essentially no problem and the "serious" emotional or behavioral problems found among 5.1% of children 15 years later.  Notice that the 1988 date was the first year in which nearly all of the children reported on would have been born during the period by which breastfeeding rates had risen moderately.  And the later data, indicating substantial serious problems, were for years in which all of the children would have been infants during a period of greatly increased breastfeeding.


Section 5:  Serious long-term outcomes related to ADHD:

It should be pointed out that ADHD is a serious problem in many ways.  According to the CDC table above, 11½% of American children in the 10-to-17 age group are diagnosed with ADHD, which means far more than 11½% of boys, since boys are diagnosed with it between 2 and 9 times as much as girls.  Not only does this condition cause difficulties in their schooling, the schooling of others, and the working lives of teachers, it also typically leads to problems in relations with peers as well as to the affected children being regularly medicated with Ritalin or other substances, long-term effects of which are very much in question.  It greatly increases the likelihood of attempted suicide in adulthood (by three to four times, according to one study, with even higher percentages engaging in intentional self-harm(18); the research cited here studied females only, but there appears to be no reason to think that the findings would not apply to males as well.  A 30-year study of 551 subjects, 72 of whom had ADHD as teenagers, found that, "compared to people without ADHD in their teens and adulthood, those with the disorder had 82 percent higher odds of having impaired physical health. They were also more than twice as likely to have another mental health problem and more than three times as likely to have antisocial personality disorder....  This behavior is often criminal in nature, according to the U.S. National Institutes of Health.  Adults with ADHD were also 2.5 times more likely to have problems at work, and more than three times as likely to have high financial stress, the investigators found."(19)


In many cases of hyperactivity in juveniles, that condition is observed to decline as a problem in later childhood. However, it is very possible that apparent improvement such as this may be only a temporary stage, during a transition toward another disorder that might be equally problematic, as indicated by a study with monkeys:  It was found that juvenile monkeys who were hyperactive later became hypoactive.(26)

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Section 6:  An historical look at the rise of ADHD in the U.S. vs. in Europe

It was pointed out earlier that the first signs of major increases in prevalence of ADHD-related symptoms in the U.S. were traceable to the 1970's; and this correlated well with the dramatic increases in breastfeeding in the U.S. beginning in the early 1970's.  However, the pattern in Europe was different in both respects, in ways that could be revealing. 


Remember from Figure 2 that breastfeeding rates in the U.S. increased sharply beginning in 1972.  And in North America in the later part of the 1970's, hyperactivity came to viewed as relatively common; "special journal issues were devoted to the topic," with the first of them appearing in 1976.  However, according to the just-quoted leading authority on the subject, hyperactivity was still considered to be uncommon in Europe at this time; and "a rapprochement between these views would not occur until well into the 1980's...."(20)  In the 1990's, there was "an expanding recognition and treatment of the disorder in countries outside the United States and Canada."(21)  Notice in the WHO/Europe chart below that a major surge in breastfeeding was at an early stage at the beginning of the 1980’s; and consider how well the rapid increases in breastfeeding that were underway in Europe at that time tracked with the history of increases in recognized prevalence of hyperactivity in Europe.

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For a more complete discussion of the above subject, including how these disorders relate to other disorders that are probably also connected with the increased exposure of infants to developmental toxins via breastfeeding, go to 




A question that should be addressed to those who are recommending breastfeeding, but which they probably won't want to answer:

Given (a) the inconclusiveness of the studies that support breastfeeding,** (b) the known concentrations of environmental toxins in recent human milk,** and (c) the many close correlations between variations in breastfeeding levels and similar variations in levels of serious childhood diseases (seen in national health data**): How do we know that breastfeeding is more beneficial than harmful?


** Supporting information and references to authoritative sources regarding matters raised in this question are included in a one-page printable version of this question, to be found at .


We have good reason to say that those who recommend breastfeeding probably will not have an answer to the above question.  A slightly different version of essentially this same question was mailed to four different high officials at the U.S. Department of Health and Human Services, who are heads of divisions that are involved in promoting breastfeeding.  As of 4 months after mailing those letters, no reply has been received.  A few months earlier, each of those officials had sent one polite response to an earlier letter that brought up the matters above, and none of their responses said anything in criticism of any of those points.  Also, variations of the above question were mailed three times to the American Academy of Pediatrics, the American Academy of Family Physicians, and the American Congress of Obstetricians and Gynecologists.  As of over 6 months after the most recent of those mailings, no responses have been received.  The points in those letters are all well substantiated.  So the question that comes at the end, above, is a logical question to ask.  But the promoters of breastfeeding appear to be unable to respond to it.  If they won't (or, more likely, can't ) answer that question as part of an informed debate on this matter (therefore to, as well as to you), should anybody pay attention to their advice?



Section 7:  Testosterone:  Its importance to neurological development, and its vulnerability to developmental toxins in human milk

Chemicals that are concentrated in human milk (PBDEs, dioxins and PCBs), and which are many times lower in bottle feedings, are known (on the basis of high-quality scientific studies) to have anti-androgenic, testosterone-reducing effects—see Sections 2.a and 3.a at for details and sources.   According to Web MD, leading effects of low testosterone are "diminishing ability to concentrate, as well as irritability and depression."  Also, quoting a urology department chairman, "diminished mental clarity, motivation, drive -- all of these things can be related to low testosterone."(9) Scientific literature points out that testosterone has important effects on mood, memory, sense of vigor and also on ability to concentrate."(10)


The psychological and mental-concentration-related effects of low testosterone have early beginnings.  Testosterone levels are typically high in an infant for several months after birth, which is probably related to their important role in development of the rapidly-growing infant brain.  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 ... (Geschwind & Galaburda, 1985; Gouchie & Kimura, 1991; O’Boyle et al., 2002)."(12) (emphasis added)   From an academic source, "recent research on animals and humans suggests that sensory perception, cognition, arousal, attention, and affective processes can be influenced by circulating sex hormones ....(Goldstein et al., 2005; Maney, 2006, Protopopescu et al., 2005; Shively & Bethea, 2004) ... Sex hormones (including testosterone) apparently influence the development of some of the same neural circuitry that is implicated in ADHD."(13) (emphasis and parenthetical expression added) 


A 2008 study found (quoting from its abstract), "high levels of circulating testosterone were related to fewer ADHD symptoms in girls."(15)    Put another way, lower testosterone levels were related to more ADHD symptoms.  Some readers might have thought that observations about effects of low testosterone (quoted earlier) would apply only to boys, but this study found that low testosterone levels apparently also have such effects in girls.  (Both genders have testosterone as well as estrogen, just in different proportions.)


Despite the apparent importance of testosterone also to female neurological development, it is probable that it has greater importance in males than in females.  Therefore exposure of infants (increasing in recent decades via breast milk) to the testosterone-lowering chemicals discussed here would be likely to have greater neuro-developmentally-toxic effects on boys than on girls. This should be kept in mind when thinking about the far higher rates of ADHD as well as autism among boys than among girls.


Dioxins are recognized to have effects related to this discussion even aside from their effects on testosterone levels.  According to the Board on Environmental Studies and Toxicology of the National Academy of Sciences, "Children and animals exposed to dioxin or PCBs in the perinatal period can exhibit various neurological disorders" including learning and memory disorders and hyperactivity.  "Yu-Cheng children (whose mothers had been exposed to elevated levels of dioxins) are rated by their parents and teachers to have a higher activity level, more health, habit and behavioral problems, and to have a temperamental clustering closer to that of a "difficult child."  Continuing with the statement by the designated board of the National Academy of Sciences, "These results indicate that a wide variety of developmental events... can be perturbed, thus suggesting that TCDD (dioxin) has the potential to disrupt a large number of critical developmental events at specific developmental stages."(16) (emphasis added)  Remember from Section 2.a the extremely high levels of dioxins in human milk, both in relation to established safe levels and in relation to levels in infant formula.


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. 



Message to health professionals and scientists reading this paper:  This author cordially invites you to indicate your reactions to the contents presented here.  As of now, new parents almost never hear anything but completely one-sided promotion of breastfeeding, with no mention of possible drawbacks except in cases of serious problems on the part of the mother.  If you feel that parents should be informed about both sides of this question and thereby enabled to make an educated decision in this important matter, please write to the author of this paper.  Also, if you find anything here that you feel isn't accurately drawn from trustworthy sources or based on sound reasoning, please by all means send your comments, to



* To read about the author of this article, go to the end after the footnotes.





(1)  Health of Generations, Jeanne Faulkner, RN  Article provided by Regence BlueCross BlueShield of Oregon, at   (Asuris Northwest Health)

(1a)  Perrin et al., The Increase of Childhood Chronic Conditions in the United States, JAMA, June 27, 2007—Vol 297, No. 24,  2755 at (2) Diagnostic controversies in adult attention deficit hyperactivity disorder. McGough JJ, et al.,  Am J Psychiatry. 2004 Nov;161(11):1948-56.

(2a) Rice et al., Critical Periods of Vulnerability for the Developing Nervous System:  Evidence from Humans and Animal Models, EPA National Center for Environmental Assessment, at, p. 515.

(2b) Grandjean and Jensen, Breastfeeding and the Weanling’s Dilemma   Am J Public Health. 2004 July; 94(7): 1075.   PMCID: PMC1448391 at

(2c) Pesticides in the Diets of Infants and Children, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C.  1993, p. 60 at

(2d)  National Research Council (U.S.). Committee on Toxicology,  Recommendations for the Prevention of Lead Poisoning in Children, p. 19, at The following direct link might work:   id=15grAAAAYAAJ&printsec=frontcover&dq=Recommendations+for+the+Prevention+of+Lead+Poisoning+in+Children&hl=en&sa=X&ved=0CB4Q6AEwAGoVChMI06yW25q2xwIVjQqSCh2dsQ2G#v=onepage&q=Recommendations%20for%20the%20Prevention%20of%20Lead%20Poisoning%20in%20Children&f=false

(3) Breastfeeding, Family Physicians Supporting (Position Paper) -- AAFP Policies -- in American Academy of Family Physicians web site.

(4) Quotation to be found at

(5) see .

(6) 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 of TEQ/kg-d)   In the EPA’s “Glossary of Health Effects”, RfD is defined:  “RfD (oral reference dose): An estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure of a chemical to the human population (including sensitive subpopulations) that is likely to be without risk of deleterious noncancer effects during a lifetime.”

(7) Infant Exposure to Dioxin-like Compounds in Breast Milk  Lorber (Senior Scientist at EPA) and Phillips  VOLUME 110 | NUMBER 6 | June 2002 • Environmental Health Perspectives (a peer-reviewed journal published by the National Institute of Environmental Health Sciences of NIH)


(7a) 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 a study at Chemosphere. 2006 Aug;64(9):1521-5. Epub 2006 Jan 25.  Weijs PJ, et al., Dioxin and dioxin-like PCB exposure of non-breastfed Dutch infants.



(7b) U.K. Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment:  COT Statement on a toxicological evaluation of chemical analyses carried out as part of a pilot study for a breast milk archive, 2004, Table 1, at


(7c) Lee et al., Association of serum concentrations of persistent organic pollutants with the prevalence of learning disability and attention deficit disorder,  J Epidemiol Community Health 2007;61:591–596. doi: 10.1136/jech.2006.054700 at


(7d)  Mocarelli et al., Perinatal Exposure to Low Doses of Dioxin Can Permanently Impair Human Semen Quality, Environ Health Perspect. May 2011; 119(5): 713–718. Published online Jan 24, 2011. doi:  10.1289/ehp.1002134  at


7e) Jens Walkowiak et al., Environmental exposure to polychlorinated biphenyls and quality of the home environment:  effects on psychodevelopment in early childhood.  Lancet 2001: 358: 1602-07  Abstract at


(8) see Section 1.b of


(8a) Barrett, Parallel Outcomes: Comparing Effects of Environmental Contaminant Exposures with ADHD in Children, Environ Health Perspect. Dec 2010; 118(12): A542. doi:  10.1289/ehp.118-a542a  PMCID: PMC3002212 at


(8b) Eubig et al., Lead and PCBs as risk factors for attention deficit/hyperactivity disorder, Environ Health Perspect. 2010 Dec;118(12):1654-67. doi: 10.1289/ehp.0901852. Epub 2010 Sep 9.  To see close connection between breastfeeding and many-times increased PCB levels, see next footnote.

(8c) Jusko et al.,  Prenatal and Postnatal Serum PCB Concentrations and Cochlear Function in Children at 45 Months of Age, Environmental Health Perspectives, 22 July 2014 (Advance Pub.), 2nd part of Table 1 near end, at


(8d)  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  

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

8f)  see for example Trnovec et al., Assessment of exposure to PCB 153 from breast feeding and normal food intake in individual children using a system approach model, Chemosphere. 2011 Dec; 85(11): 1687–1693. Published online 2011 Nov 1. doi:  10.1016/j.chemosphere.2011.09.013These authors describe several other studies that found similar results regarding PCB concentrations in relation to breastfeeding history.



 For ease of referral to the sources indicated here, if there is no highlighted link, you can (a) use your cursor to drag over and select a URL from the footnote (select the letters beginning with www or http and ending just before the next space; be sure to select all of that but no more, not even a space), then (b) control - c  (to copy that); then (c) paste that (control - v) into the horizontal web-address slot at the top left of your browser page, then press ENTER on your keyboard. 


(9)   Also p. 1 for urologist quote.

(10) Management of the Cardinal Features of Andropause,  Arshag D. Mooradian and Stanley G. Korenman  American Journal of Therapeutics 13, 145–160 (2006)  

(12)  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

(13)  see #15 below

(14) Ahlborg UG, Hanberg A, Kenne K. Risk Assessment of Polychlorinated Biphenyls (PCBs). Environmental Report in the Nord Series. Nord 26. Copenhagen: Nordic Council of Ministers, 1992.

(15)  Hormonal associations with childhood ADHD and associated trait and neuropsychological mechanisms by Martel, Michelle M., Ph.D., Michigan State University, 2008; AAT 3348153   Quotation taken from abstract at

 (16)  Board on Environmental Studies and Toxicology, National Academy of Sciences, National Academies Press: Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment (2006) p. 323

(17) , Tables 3 and 5 of Advance Data

(18) Girls With ADHD At Risk for Self-Injury, Suicide Attempts As Young Adults, Says New Research   American Psychological Assn. August 14, 2012  reported in Medline Plus Weekly Digest Bulletin, 11/25/2012

(-)  Data table for Figure 37, Death rates for leading causes of death among young adults 18-29 years of age, by sex: United States, 1980-2005  in CDC's Health United States, 2008  At   That data table can be found at


 For ease of referral to the sources indicated here, if there is no highlighted link, you can (a) use your cursor to drag over and select a URL from the footnote (select the letters beginning with www or http and ending just before the next space; be sure to select all of that but no more, not even a space), then (b) control - c  (to copy that); then (c) paste that (control - v) into the horizontal web-address slot at the top left of your browser page, then press ENTER on your keyboard. 


(19) "ADHD Can Cause Lifelong Problems, Study Finds." In HealthDay News of NIH, in Medline Plus Weekly Digest Bulletin of 12/23/12  at

(20)  Attention-Deficit Hyperactivity Disorder, A Handbook for Diagnosis and Treatment,  3rd Edition, Russel A. Barkley, The Guilford Press, New York and London, 2006, pp. 9, 19. 

(21) Barkeley, p. 35.

(22)  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


(23)  Lactational Exposure to Polybrominated Diphenyl Ethers and Its Relation to Social and Emotional Development among Toddlers  Kate Hoffman, et al., Environ Health Perspect. 2012 October; 120(10): 1438–1442. Published online 2012 July 19. doi: 10.1289/ehp.1205100  PMCID:   see text above Figure 2 in


(24) Brenda Eskenazi et al., In Utero and Childhood Polybrominated Diphenyl Ether (PBDE) Exposures and Neurodevelopment in the CHAMACOS Study  Environ Health Perspect, 2013 February; 121(2): 257–262. Published online 2012 November 15. doi:  10.1289/ehp.1205597  PMCID: PMC3569691 at


(24a) Section 5.6.2 of U.S. EPA  (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. online at  or directly at


(25) Polybrominated diphenyl ethers (PBDEs) in U.S. mothers' milk.  Schecter A, et al., Environ Health Perspect. 2003 Nov;111(14):1723-9,  found at  Other verification from Papke et al, 2001.


 For ease of referral to the sources indicated here, if there is no highlighted link, you can (a) use your cursor to drag over and select a URL from the footnote (select the letters beginning with www or http and ending just before the next space; be sure to select all of that but no more, not even a space), then (b) control - c  (to copy that); then (c) paste that (control - v) into the horizontal web-address slot at the top left of your browser page, then press ENTER on your keyboard. 


(25a) Protecting Children from Harmful Chemical Exposures Chemical Safety and Children’s Health Prepared by: IFCS FSC Working Group Chaired by Hungary  Chemical Safety in a Vulnerable World IFCS/FORUM-IV/11 INF 7 October 2003  Fourth Session of the Intergovernmental Forum on Chemical Safety Bangkok, Thailand, pp. 9-12, accessed at 

(25a1) Cheuk et al., Attention-Deficit Hyperactivity Disorder and Blood Mercury Level:  a Case-Control Study in Chinese Children  Neuropediatrics 2006; 37: 234–240  at


  (25a1a) Winneke, Neurobehavioral Toxicity of Selected Environmental Chemicals: Clinical and Subclinical Aspect, at Behavioral Measures of Neurotoxicity: Report of a Symposium, at



(25a2)  P. Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants,  Environmental Health Perspectives, accepted Oct. 1993


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 


25a3) U.S. ATSDR document on mercury at, p. 443, showing estimate of 8 ppb.


Code of Federal Regulations, Title 21, Chapter 1, Subchapter B, Part 165, Subpart B, Sec. 165-110 at, showing maximum allowed of 2 ppb


25a4) Lind et al., Breastfeeding and Later Psychosocial Development of Children at 6 Years of Age, Pediatrics Vol. 134 No. Supplement 1 September 1, 2014, pp. S36 -S41 (doi: 10.1542/peds.2014-0646G)    at,  citing Breastfeeding and subsequent social adjustment in six- to eight-year-old children. J Child Psychol Psychiatry. 1987;28(3):379–386pmid:3597562


25a5) See chart in Kevin Pollard, The Gender Gap in College Enrollment and Graduation, Population Reference Bureau, at


25a6) Joseph Chamie, Women More Educated Than Men But Still Paid Less, Yale Global Online, March 6, 2014, at


(25b)  Polańska et al., Exposure to Environmental and Lifestyle Factors and Attention-Deficit / Hyperactivity Disorder in Children – A Review of Epidemiological Studies,   International Journal of Occupational Medicine and Environmental Health 2012;25(4):330 – 355 DOI 10.2478/S13382-012-0048-0   at


 For ease of referral to the sources indicated here, if there is no highlighted link, you can (a) use your cursor to drag over and select a URL from the footnote (select the letters beginning with www or http and ending just before the next space; be sure to select all of that but no more, not even a space), then (b) control - c  (to copy that); then (c) paste that (control - v) into the horizontal web-address slot at the top left of your browser page, then press ENTER on your keyboard. 


(25c)  M A Mascola,et al.,  Exposure of young infants to environmental tobacco smoke: breast-feeding among smoking mothers.  Am J Public Health. 1998 June; 88(6): 893–896. PMCID: PMC1508233  found at   


(25d) 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


25e)  Re:  RfD of PBDEs:- 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


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:


25f) Re:  Mercury levels in breast milk:  U.S. ATSDR document on mercury at, p. 443

-  Re:  mercury levels allowed in bottled water:   Code of Federal Regulations, Title 21, Chapter 1, Subchapter B, Part 165, Subpart B, Sec. 165-110 at


25g) Re:  PCB levels 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


25h)  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


25i) 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.



 25j)  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


25k)  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 this study provides a range of  52 to 2455 ng/kg fat, which equals .05 to 2.45 ng/g fat (lipid)  (Krokos et al., Levels of selected ortho and non-ortho polychlorinated biphenyls in UK retail milk, Chemosphere. 1996 Feb;32(4):667-73.  at






(26)  Bowman RE, Heironimus MP.  Hypoactivity in adolescent monkeys perinatally exposed to PCBs and hyperactive as juveniles. Neurobehay Toxicol Teratol1981 ;3:15-18.

(27)  S Patandin et al.,  Effects Of Environmental Exposure To  Polychlorinated Biphenyls And Dioxins On  Growth And Development In Young Children:  A Prospective Follow-Up Study Of Breast-Fed And Formula-Fed Infants From Birth Until 42 Months Of Age    Table 7.5   at   http://Repub.Eur.Nl/Res/Pub/19721

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


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


Don Meulenberg

Fredericksburg, VA, USA