Developmental Toxins in Breast Milk vs. those in Infant Formula


According to leading experts in this field, many toxic substances that have become widespread in environments of developed countries “have caused contamination of human milk only during the last half century, and long-term health impacts are now being discovered."(1)  Research has found over 350 different pollutants in human milk. (2)  It has been widely recommended that women breastfeed their infants, and those recommendations were well-founded in earlier generations; but the time has apparently come for those recommendations to be reconsidered. 


Breastfed infants have been found to normally be exposed to mercury at levels several times higher than the maximum allowed by U.S. law in bottled water (2a).  The reasonably-safe upper threshold of daily exposure to the neuro-developmental toxin and carcinogen, dioxin, (as determined by the EPA) is 0.7 pg TEQ/kg-day (picograms toxic equivalency per kilogram of body weight per day);(3)  this should be compared with the body-weight-based dose received by an apparently typical breastfeeding U.S. infant at initiation of nursing, which was found to be more than 300 times that estimated safe exposure, at 242 pg TEQ.(4)  Levels have been found to be similar in the other developed countries for which data is available.(5)  Infants are exposed to these toxins at the developmentally most vulnerable times of their lives, while their brains are rapidly growing, while their immune systems would normally be developing properly, and just before a period when childhood cancer is unusually likely to become evident.  Formula-fed infants are exposed to these toxins in concentrations scores to hundreds of times lower than the concentrations in breast milk.(6)


Various studies have found benefits of breastfeeding, but studies have found conflicting results on many major questions, for various reasons; over 50 scientific studies have found that worse health outcomes were associated with breastfeeding or greater duration of breastfeeding.(7)  Among others, a study of all 50 U.S. states and 51 U.S. counties found that "exclusive breast-feeding shows a direct epidemiological relationship to autism," and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism."(8)


The above was summarized from material that is presented in much greater detail at another website,, on the same general topic to which this website is devoted.  Here are some other points and section headings from the remainder of that other article:


Many-times higher infant intake of toxins from breast milk than from formula or from trans-placental exposure:


Section 1.a:   Dioxins and PCBs, recognized neuro-developmental toxins, in doses scores to hundreds of times higher than in infant formula.   "Significantly more (10 to 20 times) of a mother's body burden of persistent organohalogens is transferred to the infant via the milk than by the transplacental route." 


Section 1.b:   PBDEs, neuro-developmental toxins with potent estrogenic effects, almost 10 times higher in urban air than in rural air, and present in breast milk in concentrations over 50 times higher than in infant formula.


Section 1.c:  Mercury, and brain development taking place after birth, Part 1.  Concentrations in human milk over 100 times higher than infant formula; ingested by the infant at an extremely vulnerable time for his or her neurological development; 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; many studies finding associations of autism with mercury levels less than twice the normal range; over twice as much growth and development of the brain (the stage of greatest vulnerability to toxins) takes place in the year after birth as takes place before birth.


Section 1.e: Specific mercury concentrations, breast milk vs. formula, and compared with a U.S. government maximum.  More than 300,000 American newborns every year are considered by the EPA to already be at risk of neurological harm based on prenatal exposure alone, according to the EPA.  Then, during a period of continued vulnerability of the rapidly developing brain to toxins, infants ingest either a food that could triple their mercury levels within one year (human milk) or a food that is less than 1% as high in mercury as the first alternative.  Dramatic increases of mercury in modern times.


Section 1.f  Lead:  A study of breastfeeding duration and infant blood lead reported that longer breastfeeding was associated with higher infant lead concentrations in three countries, in three different decades, and in settings with differing breastfeeding patterns, environmental lead sources, and infant lead levels


Section 1.g:  Other chemicals reported in human milk, comparing their concentrations with those in cows' milk, including phthalates, perchlorate, PFOA, PFOS, cadmium, and aluminum


Section 1.h:  Conspicuous effects of lactational exposure to developmental toxins, as opposed to effects only from gestational exposure:  evidence of diseases’ incidences increasing in proportion to the duration or exclusiveness of breastfeeding


Section 1.i:  Breastfeeding and smoking

-- Ten times increase in breastfed infant’s exposure to smoking toxins.


Much greater detail on all of the above will be found at


Here is a table of contents of what follows in this website:

Section 1: Dioxins, PBDEs, PAHs and BPA acting as Developmental Toxins (Endocrine Disruptors), Carcinogens, and Mutagens

Section 1.a:  Nature of the harm caused by these chemicals:  Endocrine disruption, reduction of thyroid and testosterone that are essential for proper brain development

     1.a.1:  Disruption of development of the immune system

     1.a.2:  Effects of PBDE exposure related to ADHD and other mental disorders

     1.a.3:  Harm to postnatal formation of connections in the brain, important in autism;

Section 1.b:   Sources of these toxins:

Section 1.c:  Typical breast milk these days is very different from that of earlier times

1.c.1:   Increases of Dioxins  -- PCBs

1.c.2:   Increases in mercury

1.c.3:   Especially large recent increases in PBDEs in human environments: 

1.c.3.a    100-fold increase in human exposure to endocrine-disrupting BPA (Bisphenol A)

1.c.4:   Diesel emissions and inhalation of toxins in developed areas.


Section 2:   More on how these toxins harm development

Section 2.a:   Effects of dioxins, PCBs and mercury in human milk

Section 2.b:   Pesticides, bromine and phthalates


Section 3:  Synergistic effects resulting from combined exposures to multiple toxins at low doses in breast milk



Section 1:

Dioxins, PBDEs, PAHs and BPA acting as Developmental Toxins (Endocrine Disruptors), Carcinogens, and Mutagens

In the words of the U.S. Agency for Toxic Substances and Disease Registry, with emphasis added:  "The proper development of many systems and functions (in an infant) depends on the timely action of hormones...; therefore, interfering with such actions can lead to... altered metabolic, sexual, immune, and neurobehavioral functions.  Effects of this type...occur following exposure....early in life caused by either direct exposure to chemicals or exposure (to environmental chemicals) via maternal milk."(9) (The text segments that applied directly to the present discussion were selected from the original text; the complete text can be found at the footnote shown.)


Section 1.a:  Nature of the harm caused by these chemicals:

One important form of dioxins is a known carcinogen, other forms of dioxins are classified as likely carcinogens, and PAHs are well known to cause cancer in animals.  One specific means by which dioxins, PBDEs, BPA and at least one PAH cause neuro-developmental harm is by acting as "endocrine disruptors."   A web page of the National Institutes of Health says that endocrine disruptors are "chemicals that may interfere with the body’s endocrine system and produce adverse developmental, reproductive, neurological, and immune effects in both humans and wildlife. …. ." (emphasis added)   Some PAHs have been identified as mutagens, which can have adverse effects on the ways organs including the brain develop.


Quoting from the NIH's web page on endocrine disruptors, "Endocrine disruptors …may mimic or interfere with the function of hormones in the body. Endocrine disruptors may turn on, shut off, or modify signals that hormones carry,…" Continuing, "Research shows that endocrine disruptors may pose the greatest risk during prenatal and early postnatal development when organ and neural systems are developing.”  Specific toxins mentioned are dioxins, PCBs, BPA and other plasticizers, and DDT.(11)    According to the Committee on Developmental Toxicology of the National Academy of Sciences, ”Agents that interact with one or more of these receptors and are known to produce abnormal development include ……dioxin (TCDD)."   Explaining how dioxin affects the developing body, the NAS committee points out that it "... alters the expression of several dozen genes, one or more of which might result in an adverse developmental outcome."(12)  (emphasis added) 


First note that, according to a 2008 EPA report, “It is known that thyroid hormones are essential for normal brain development in humans and that hypothyroidism (low thyroid) during fetal and early neonatal life may have profound adverse effects on the developing brain (Morreale de Escobar et al., 2000; Haddow et al., 1999).”(12b)(italics added)  Then be aware that ten studies were cited in support of the statement that “among the pollutants, PCBs (PCBs are chemical relatives of dioxins) and dioxins have dramatic effects on TH (thyroid hormone) function in humans ….  PCBs have been shown to decrease circulating TH levels during development.”(12c).  A 1998 Japanese study was especially relevant:  Effects of postnatal exposure to dioxins and PCBs were studied in 36 breast-fed infants. Estimated intakes of these chemicals from the breast milk “significantly and negatively correlated” with the levels of thyroid hormones in the blood of breast-fed babies.12a   All of the above should be seen in relation to the finding that human milk is typically over a hundred times higher in dioxin and 25 times higher in PCBs than infant formula, at initiation of breastfeeding (see Section 1.a  of


Regarding PCBs specifically A 2012 study referred to by the NIH described evidence suggesting that "...PCBs are environmental risk factors for ASD.”  And continuing, “There is experimental evidence that developmental exposure to PCB-95 elicits some aspects of ASD, including an imbalance between excitation and inhibition in the auditory cortex of weanling rats (Kenet et al. 2007) and altered social behaviors in rats."(13)


One substantial study found harmful effects of PCBs transferred to human infants specifically by breastfeeding.  A large team of German scientists and physicians, studying 171 healthy mother-infant pairs, found "negative associations between (human) milk PCB and mental/motor development ... at all ages, becoming significant from 30 months onwards."  Also, "negative associations with PCB increased with age."  They based their observations on data both from the breastfeeding period (PCB concentrations in the milk times the number of months of breastfeeding) and from measurements of serum at 42 months of age (recognizing that most of a breastfed child's PCB levels at 42 months would have resulted from PCBs transmitted in breast milk). They found no significant association of the children’s neurological development with PCB levels in umbilical cord blood.(14) 


One logical explanation for greater long-term effects of PCBs has been provided by the determination that PCBs disrupt the blood brain barrier, as determined in studies published in 2010 and 2012.(15b)  This leaves the brain more vulnerable to background environmental toxins to which the child is gradually exposed over the course of many years; and this would clearly have mainly long-term rather than short-term effects, especially considering that the most seriously-implicated neurodevelopmental toxins (dioxins, PCBs, PBDES, and mercury) accumulate in the body over time.


A 2007 study (Lee et al.) was apparently the only study that has been carried out on the association between background exposure to persistent organic pollutants (POPs) and clinically significant developmental disorders, such as learning disability or attention deficit disorder, among children from a general population.  The authors found dramatically increased odds of 12-to-15-year-old children’s having these disorders if they had detectable levels of dioxins or furans.  The average odds ratio of having Learning Disability for those with detectable levels of dioxins/furans, compared with those without detectable levels, was 2.33 (that is, a 133% increased likelihood); and the average odds ratio of having Attention Deficit Disorder for those with detectable levels of dioxins/furans, compared with those without detectable levels, was 3.02 (three times as likely).  For more about this study, go to Section 2.a.   


A 2013 review article about ADHD-related effects of pesticides and PCBs summarized various studies as follows:  “Exposures to organochlorine pesticides and PCBs were associated with ADHD-like behaviors….”(15c)


Another German study (Winneke et al.) found that, in two out of three testings at 30, 42 and 72 months after birth, cognitive deficit was found to be induced by “perinatal exposure to polychlorinated biphenyls (PCBs).”  The examination at 72 months was the one that found no cognitive deficit resulting from the perinatal exposure, which should be seen in light of the fact that this was the least valid of the three tests, since 23% fewer children in the group were tested at 72 months.(15)  There is good evidence of long-term detrimental effects of this known developmental toxin. (see Section 1.d in 


A mere 1/800,000th of an ounce was the amount of a PCB-containing product administered per day to pregnant or lactating female monkeys that was found to cause the offspring to be hyperactive and retarded in learning ability.(see Section 2.a)   According to an expert study, “There is excellent correspondence between the effects of developmental PCB exposure in the monkey and that observed in humans, including learning deficits and changes in activity.”(15a)   

PCBs are highly concentrated in human milk, and only in low concentrations in infant formula (see Section 1.a in  For summaries of other studies finding neurological harm to result from exposure to PCBs, see Section 2.d  in www.breastfeeding-studies.infoTo see charts showing how great the increases of PCBs in a child’s body are as a result of breastfeeding, see Figure 3 and Figure 4 later in this article.



Section 1.a.1:  Disruption of development of the immune system is another serious probable consequence of the above chemicals, as well as a consequence of other chemicals known to be in human milk:  According to an extensive 2011 study on environmental toxicants and the developing immune system, toxins including dioxins, PCBs, PAHs, BPA, and phthalates can harm development of the immune system.  A 2007 study listed those plus other environmental toxicants seen to harm development of an infant's immune system, including heavy metals, tobacco smoke, and pesticides.(16)  Note that all of the above toxins (or, in the case of tobacco smoke, components of that toxin) have been found in breast milk; as mentioned, dioxins have been found in human milk in doses scores of times higher than the EPA-determined safe level, or hundreds of times higher at initiation of typical breastfeeding in the U.S.(3,4)  Moreover, according to the most authoritative data that appears to be available, the doses of these toxins in human milk have been found to be scores to hundreds of times higher than those in infant formula.(17)


Of special relevance regarding sexual development, "Most PBDEs have antiandrogenic activity; tetra- to hexa-BDEs have potent estrogenic activity in vitro; hepta-BDE and 6-OH-BDE-47, a metabolite of BDE-47, have anti-estrogenic activity."(20)  Important gender-related development takes place not only in infancy but also, obviously, during adolescence, such that there should be concern about extensive teenage exposure to these anti-androgens, anti-estrogens and often-potent estrogenic toxins via large amounts of time spent close to electronic devices (the main source of PBDEs).  Section 1.c.3 tells about the especially rapid increase of PBDEs in human environments and human tissues during recent decades.


A 2012 study reported that its "findings suggest an association between PBDE concentrations in colostrum (early breast milk) and impaired infant cognitive development."(21)  The authors also pointed out that “in the group of children breastfed for a longer period the association between BDE-209 exposure and neuro-development impairment was somewhat stronger….  Further, associations in the longer breastfeeding group may be underestimated because the higher social class and education level of these mothers may provide a more advantageous environment for neuro-development.” 


According to a Japanese study, "Several toxic effects on the thyroid system or on neurodevelopment have been reported in experimental animals exposed to PBDEs." (23)  Note the expert statement that “any agent (such as PBDEs) that disrupts normal hormone secretion (such as that of thyroid, which is known to be important to neurological development) can upset normal brain development.”(23a) (parenthetical expressions added)   A 2012 review study states, “PBDEs are known to affect thyroid hormone (TH) levels which in turn are known to affect neuronal differentiation, migration, myelination, synaptogenesis and dendritic branching.”(23b)



Section 1.a.2:  Effects of PBDE exposure related to ADHD and other mental disorders: 

(1) A 2012 study found that children who had consumed breast milk that was merely in the two upper quartiles in PBDE levels 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;(24)  

(2) a 2011 Spanish study estimated the effects of postnatal exposure to PBDEs in children 4 years of age, finding that children with higher PBDE concentrations had greater attention deficit symptoms, general cognitive deficits, and poor social competence (160% increased risk);(25) and

(3) according to Italian scientists, “the main hallmark of PBDE neurotoxicity is a marked hyperactivity at adulthood. Furthermore, a deficit in learning and memory processes has been found at adulthood in neonatally exposed animals.”(26)



It should be noted that both of the latter two studies discussed just above were done in Europe, where PBDE levels are many times lower than in the U.S., yet ADHD-like and other mental effects were nevertheless of very serious concern.


A 2013 study that was described by its authors as “the largest study to date on the potential neurodevelopmental impacts of PBDE exposures” arrived at relevant findings on this topic:  it was found that increased PBDE level in a 7-year-old child was associated with a 4.5 times higher odds of the child being rated by the teacher as being in the “moderately or markedly atypical” range on the standard Hyperactive/Impulsive subscale, and with a 5.5 times higher risk of the child being rated as moderately or markedly atypical in the scale for general mental disorders.(27a)  The increased PBDE level in the children that was found to be associated with those specific risks was a ten-fold increase, which may sound like an unusual amount, but it is not; it is well established that, as stated by experts G. Giordano and L.G. Costa, “Levels of PBDEs have significantly increased in the past decades, and those in human tissues in North America have been consistently found to be one to two orders of magnitude (10 to 100 times) higher than those reported in Europe and Asia.”(27b)  (The higher levels in North America were due largely to U.S. requirements until 2013 for using fire retardants in many household and office products, including electronics, which products will continue in use for many years.)


PBDEs are considered to be endocrine disruptors, interfering with normal development of the brain.  According to a review of PBDEs as risk factors for autism, they "are particularly close chemical analogs of thyroid hormone, a major timing factor for the precise regulation of brain cell growth and connectivity that appears aberrant in ASD."(27)  Several studies have been done with animals that received developmental exposure to PBDEs, enabling the above-quoted reviewer to summarize, "the fact that so many different replications and combinations showed alterations of adult behaviors after early life exposure supports a hypothesis that PBDEs have a significant potential for disruption of normal neurological development."(27)


First remember from two paragraphs earlier that 10-fold and even far greater differences in PBDE levels in humans are commonplace in the general population.  Then note that a 2010 study found that a 10-­fold increase in umbilical cord serum BDE-47 was associated with a 5.5-point decrease in Full Scale IQ at age 4 years.(27c)  A 2013 study found very similar results at age 4 (4.7 point decrease with a 10-fold increase in cord BDE-47.)(27a)  A 2014 study found similar results with regard to IQ at age 5 (4.5 point decrease with a 10-fold increase in total PBDEs) but also significant increases in hyperactivity.(27d)  The relationship between developmental PBDE exposure and reduced IQ therefore appears to be well established, with very similar findings in multiple studies.  


If a difference of about five points in IQ with a 10-fold increase in PBDE exposure doesn’t sound very serious, note that this could be a very understated way of describing the apparent effect on many children, since American children have been found to have up to 100 times the exposure of European children to PBDEs.(27b)


Some of the above-cited studies referred to associations with “prenatal” exposure to PBDEs; “prenatal” exposure is typically measured in umbilical cord blood and/or in breast milk.   It is probable that a mother’s exposures to dust from fire retardants in interior furnishings and electronics (principal sources of PBDE exposure) would be relatively stable; therefore her PBDE levels measured prenatally or in cord serum would be very similar to those not much later in her breast milk, to which most infants are exposed these days.  The significance of that is especially great considering that PBDEs are known to become highly concentrated in breast milk.  (Read on.)


The above well-substantiated adverse effects of developmental exposure to PBDEs should be seen in combination with the finding that breast milk is typically over 30 times higher than infant formula in PBDE content.(27b11)


Details about scientific determinations of neuro-developmental effects of dioxins and PCBs will be presented later, in Section 2.a .


Section 1.a.3:  Harm to postnatal formation of connections in the brain, important in autism:

Neurons are building blocks of the brain, but they serve their purposes only by way of connections between neurons (comprised mainly of dendrites, axons and synapses).  In a study published in 2014, the authors stated that a recent meta analysis of 25 studies reported data “supporting the theory of specific underconnectivity in autism focused on tracts supporting auditory information and language processing.”  Using DTI (diffusion tensor imaging), the authors found that both SPD (Sensory Processing Disorder) and ASD cohorts demonstrated decreased connectivity in brain tracts involved in sensory perception and multisensory integration.  And they found that the ASD group alone shows impaired connectivity, relative to controls, in temporal tracts thought to subserve social-emotional processing.”(27b2)  A 2009 study in Environmental Health Perspectives (Yang et al.) noted, based on many studies, that “Neurodevelopmental disorders are associated with altered patterns of neuronal connectivity.(27b9)


Given the above very substantial evidence linking impaired connectivity with neurological disorders, it is important to focus on when development of the connections takes place.  It turns out that this process is overwhelmingly postnatal, and more specifically, early postnatal.  According to a 2009-2010 study, “perinatal and early postnatal brain development features the onset of myelination and a striking development of gray matter connections, especially in sensorimotor and visual cortices.”(27b3)  The authors support their statements about rapid postnatal formation of connections with citations of several studies employing MRI and postmortem examinations.  The tremendous extent of postnatal formation of connections is indicated in a publication of the Life Sciences Learning Center of the University of Rochester, explaining that, When a baby is born, she has about 100 billion brain cells with short axons and few connections to other neurons. From birth to age 2, new synapses (important components of connections) form at the rate of up to 2 million new synapses each second.(27b4)

Given the strong linkage of impaired connectivity with harmful outcomes of ASD (as well as SPD), and the predominantly postnatal timing of the formation of connections within the brain, we should consider the role of environmental toxins in reducing connectivity in the developing brain, postnatally:

Heavy metals (including mercury):  According to a publication of the National Scientific Council on the Developing Child, on a Harvard University website, At levels frequently measured in our environment, heavy metals interfere with the construction of the basic framework of the maturing brain as well as with its function. These toxic effects include disruption of neural cell migration from one part of the brain to another, as well as the formation of synapses….”(27b5)   In that regard, note that 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.(27b6) This finding was very compatible with other information compiled by an EPA-contracted research group(27b7) and also with the over-200% increases due to 6 months of breastfeeding as found in another study.(27b8)


PCBs:  The Yang et al. study referred to above(27b9) concluded that “Developmental exposure to PCBs interferes with normal patterns of dendritic (connection-forming) growth and plasticity.”  Relevant to that, note that PCB levels in breastfed children have been found to be extraordinarily high in comparison with bottle-fed children, especially with longer durations of breastfeeding. (see Fig. 4 and text below it)


PBDEs:  A 2012 review study states, “PBDEs are known to affect thyroid hormone (TH) levels which in turn are known to affect neuronal differentiation, migration, myelination, synaptogenesis and dendritic branching.”(27b10)  Related to that, it is worth noting the differences in PBDE concentrations found in breast milk vs infant formula -- over 30 to 1 -- as indicated by authoritative sources.(27b11)



Section 1.B   Sources of these toxins:

(a) dioxins are unintentional byproducts of several industrial chemical processes and of most forms of combustion, including wildfires, backyard burning, municipal solid waste and industrial and hospital incineration, vehicle exhaust (mainly diesel emissions), and emissions from oil- or coal-fired power plants, and are also found in weed killers and in ordinary soil onto which dioxins have settled out of the atmosphere; animal fat in the diet accounts for close to 90% of dioxin exposure in the United States, according to a 2003 National Academies of Science report on dioxins in the food supply.(28)  A study in India found that milk from mothers who lived near waste disposal sites was 2 to 5 times higher in dioxins than average.  Vegetarians are reported to consume only 2 percent of the dioxin load of the general population, because their diet is dominated by foods low on the food chain. (30)


(b) PAH's are also unintentional products of typical forms of combustion, including cigarette smoking, residential wood burning and vehicle emissions.  (Note that most of the above sources are related to population density and combustion processes.) 


(c) As mentioned, most human intake of PBDEs comes from dust released by electronic devices within homes and buildings.  They are essentially used as fire retardants in consumer plastics, especially electronic devices such as TVs and computers, but also carpeting and drapes. 


(d) Human exposure to BPAs comes mainly from plastic packaging of food and metal cans.


(e) Mercury:  Aside from the predominant sources in seafood and dental amalgam, there are many other sources as discussed in the Appendix.




Section 1.C    Typical breast milk these days is very different from that of earlier times:

 1.C.1   Increases of Dioxins:

 1) Estimates from various studies suggest that rates of dioxin deposition in the environment (mostly from the air) increased more than 10-fold between the 1930s and the late 1960s. (31)  Smokestack sources of new dioxin emissions have declined recently, but sources in the U.S. that reach populated areas intensively (dioxins in diesel emissions) have continued to greatly increase, as of the most recent EPA data. (32)   Although the rate of increase in the environment has slowed, those "persistent" toxins continue building up in soil, and from there typically return to the air, water and food supply.  Remember from the introductory paragraphs how far dioxin contents of typical breast milk have been found by the EPA to exceed the EPA's estimated safe level, and also bear in mind from Section 1 how greatly a breastfed infant's ingestion and accumulation of PCBs and other forms of dioxins exceed those of an infant that has not been breastfed.


2) The average dioxin contents of animal-based foods is much higher than in earlier times, following the increases of toxins in the environment. The U.S. Agency for Toxic Substance and Disease Registry says that "eating food, primarily meat, dairy products, and fish, makes up more than 90% of the intake of CDDs (dioxins) for the general population." (33)  Farm animals and fish ingest and build up persistent toxins in their tissues largely as a result of what they eat, meaning vegetation and sediment onto which the greatly-increased levels of dioxins and mercury from the environment have been deposited.   Moreover, meat consumption has more than doubled in the United States in the last 50 years,(34)  while the population only increased 72%. 


3)   It is probable that diesel emission pollution will continue to increase in the U.S., as more and more decades-old diesel-powered vehicles (with their worsening emissions) continue in operation in the U.S. without emission restrictions, unlike in the EU countries where required annual emissions inspections are standard.  (Note that, in addition to typically consisting partly of dioxins, diesel emissions as a whole are known separately to be both endocrine disruptors and carcinogens.)  Backyard burning (including its typical major component of plastics trash, which contributes to formation of dioxins) is difficult to control and became the largest single source of dioxin releases in the U.S. environment as of the latest EPA inventory (for year 2000).  The worst effects of the pollution generated would be on infants and child-bearing women living in the areas near where the burning is done, but the dioxins released would also enter the food chain of the general population (this burning is mostly done in rural areas).  The emissions released would also be deposited on soil, water supplies, and in the form of dust, to which all infants downwind could be exposed. 


PCBs:    PCBs are typically considered to be related to dioxins, and they (like dioxins) have neuro-developmentally toxic and carcinogenic properties.  They were banned from production for most uses in the U.S. and most European countries in the late 1970's, so proponents of breastfeeding point to that as an illustration of how hazards from breast milk have been decreasing in recent decades.  But unfortunately these and similar toxins are classified as "persistent" for good reasons, partly because of their very long lives, partly (in the case of PCBs) as a result of their leaking from old equipment, and partly because they continue to be generated unintentionally by combustion processes, including the ever-increasing diesel emissions. 1

An illustration of people trying hard to see decline of harmful toxins in breast milk:

This chart shows PCB levels detected in human milk during the period 1992 to 2007 in a group of mostly-European countries, with a downward-sloping line that is an attempt to show a long-term reduction in seriousness of breast milk's toxicity.  A careful examination of the data would require first looking at the data points through 2002, which includes most of the period shown and the overwhelming bulk of the data; this section shows nothing but an upward trend.  After that, the only low data points were

   a) the one in 2003 for a country for which no earlier data was shown (therefore this provided no indication of a decline) and

    b) the three in 2007; of those three, only one showed a decline in PCB levels compared with its earliest reading.  (See the bottom points for the years 1992 and 2000 for earlier readings for the other two -- the bottom point in 1992 is of the same country whose data point is largely covered by the median mark in 2007.)  (The low resolution/low legibility is as this chart was displayed in the summarized version of the study showing it.)  So, on the basis of what was actually only one decline in the reading for only one country out of 14 in the chart, the authors showed a conspicuous trend line depicting a substantial general decline in PCB levels during this entire period.


One might get the impression that some people are eager to find an indication that toxicity of contaminants in human milk is declining, but are having a hard time finding valid support for that idea.


1.C.2   Increases in mercury:

According to the EPA, mercury in the ­atmosphere tripled between the era before human activity and current times, (36)  and it continues to be emitted by many combustion sources (especially coal-fired power plants).   Study of samples of mercury concentrations in marine animals showed average twelve-fold increases between the mid-to-late 19th century and the end of the 20th century, and there have been signs of a particularly rapid increase after 1970.(37)  As reported in a major 2006 academic report, “research shows that mercury levels in the food chain are increasing.”(37a)


1.C.3   Especially large recent increases in PBDEs in human environments: 

PBDEs didn't come into use until the 1960's and 1970s. (38)  As of a 2007 report, "during the last 30 years, PBDE levels in humans have doubled about every 3 to 5 years and continue to increase." (39)  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.(40)   PBDE concentrations in human milk in Canada were found to increase 7-fold between 1992 and 2002.(41)  As of a 2006 study, PBDE levels in human milk measured in Europe had also been continuing to increase fairly rapidly.(41a)


Note in Section 1.7.1 at  about endocrine-disrupting, anti-androgenic, testosterone-reducing effects of PBDEs, which are already at levels that greatly affect likelihood of a child's having ADHD, even while levels in humans are rapidly increasing.  And remember from Section 1.b the data showing PBDEs to be in concentrations over 50 times higher in human milk than in infant formula. 


Bear in mind that, while current exposure just to PBDEs alone is rapidly growing and very often likely to be at toxic levels, that is without even mentioning the other toxins that are also known to be present in breast milk


1.C.3.a    100-fold increase in human exposure to endocrine-disrupting BPA (Bisphenol A)

BPA is another recognized endocrine disruptor, to which people including future mothers and nursing mothers are especially exposed via its use in plastic packaging of food and drinks, including in linings of metal cans. Production of BPA in the U.S. increased over 100-fold between 1991 and 2004.  The National Toxicology Program (NTP) has “some concern” for effects on the brain, behavior, and prostate gland in fetuses, infants, and children at current human exposures to BPA.  The U.S. Geological Survey is confident that adult exposure to BPA affects the male reproductive tract, and that long-lasting effects in response to developmental exposure to BPA occur in the brain, male reproductive system, and metabolic processes.(42)  The NIH reports that BPA can be found in breast milk.(43)


1.C.4   Diesel emissions and inhalation of toxins in developed areas:

Considering that dioxins from diesel emission have been increasing greatly (doubling in U.S. emissions in the last 13-year period reported on in the latest EPA data), it is very likely that diesel emissions in general have also been increasing substantially.  Note that diesel engine exhaust was classified as a known human carcinogen by the EPA in 2012.   One of the other toxic components known to be contained in the increasing diesel emissions, PAHs (known to cause cancer in animals), has almost certainly also continued to increase in atmosphere inhaled by many nursing mothers and mothers-to-be.  Note in the next paragraph how closely PAH concentrations in breast milk are related to exposure to diesel exhaust.

Fig. 2

This chart (from a Japanese study) indicates high concentrations of five different kinds of PAHs in breast milk of rats that had been exposed to diesel exhaust for six hours a day from the seventh day of gestation until 14 days after birth, with concentrations similar to those in downtown Kanazawa, Japan (44)  (Kanazawa is the study's lead author's university city, population 450,000).  As indicated in this chart, PAH concentrations in the breast milk of the diesel-exposed rats ("DE") were two to three times higher than in the control group, despite the fact that the exposure was apparently only moderately high; note that this exposure of the rats to downtown-level diesel exhaust, for only six hours a day, was not an especially high dosage.  Lactation appears to be an efficient means of taking in toxins from the atmosphere and concentrating them in breast milk.  Although information about PAHs in cow's milk does not appear to be available for comparison, it is probably safe to assume that a much higher percentage of human mothers and mothers-to-be than of cows has a close exposure to diesel exhaust, from vehicular traffic, railroads, ships, port and canal dredging machinery, construction equipment, etc.


An Italian study found PAHs to be much higher in lactating women who smoke.  The specific form of PAH that was investigated in this study was benzo(a)pyrene (BaP), which is classified as a Class 1 carcinogen by the International Agency for Research on Cancer.  There is no determination of a maximum tolerable amount in breast milk, so the Acceptable Daily Intake (ADI) for drinking water was used in the study. "For babies whose mothers belonged to the non-smoker rural category, daily BaP equivalent intake during a six-month nursing period was below the ADI."  But intake of BaP in breast milk by infants of urban smokers showed values "from about seven times, up to 1000 times higher than ADI." (emphasis added)  Breast milk of urban non-smokers was intermediate in concentrations.(45)  Note that BaP is also a major component of diesel exhaust,(46)  as well as of tobacco smoke, both of which are separately known to be carcinogenic. 


Authorities writing about dioxins, which are better known than PAHs, emphasize the predominant role of diet as being the major source of those toxins into the body (and thereby into breast milk).  It is worth taking special note of the fact that, in the cases of the also-toxic PAHs from diesel exhaust and tobacco smoke (as indicated above) and PBDEs from electronics, the inhalation route is also an important means of absorbing environmental toxins which can then become highly concentrated in breast milk.  In that regard, remember from earlier that PAHs are not only carcinogens but some of them are also endocrine disruptors, capable of damaging neurological development. 


The above two studies appear to be the only ones published regarding presence in breast milk of PAHs (including BaP).  They show carcinogens and probable developmental toxins being found especially concentrated in breast milk following rather ordinary exposures of the mothers to vehicle emissions and tobacco smoke.  The amount of PAHs in the breast milk was directly related to the extent of the mothers' exposures to the chemicals. The finding of carcinogenic intake of BaP by breastfeeding being up to 1000 times the acceptable level for infants of urban smoking mothers, while levels were in the safe range for rural non-smokers, highlights how extremely effective lactation is at taking in environmental pollutants in typical amounts and concentrating them in breast milk. 


Regarding the rapidly-increasing dioxins from diesel emissions, typically reaching closely into populated areas, those emissions are probably a major part of what underlies the doubled risk of autism found among infants residing within about 1000 feet of freeways in a California study.(47)  (Diesel emissions are known to be many times higher than unleaded gasoline emissions in dioxin content.)(48)  If autism risk is doubled near high-traffic roads, shouldn't we consider with caution an infant food source that dramatically increases in developmental-toxin content when that food source is located near high-traffic areas?  Especially considering that infant ingestion of toxins is scores of times higher via breast milk than via inhalation.(49)  That should even more be the case if there are alternative infant food sources that are known to typically be many times lower in concentrations of known developmental toxins, as a logical consequence of coming from animals that consume low-toxin, herbivorous diets and that live outside urban areas. (see Section 1 above) 


Although the above-cited studies measuring toxins in human milk dealt with PAHs, it is worth thinking also about other known carcinogens and developmental toxins known to be concentrated in human milk, specifically dioxins.  The National Academy of Sciences estimates that animal fat in the diet accounts for close to 90% of dioxin exposure in the United States.   In the absence of information to the contrary, diet should therefore be the exposure avenue of greatest concern, by far.  If many or most infants ingest a diet that consists exclusively of a substance (human milk) known to contain (in contemporary developed countries) very high levels of developmental toxins, that diet ought to receive careful scrutiny.  One appropriate kind of scrutiny would be to look at each of the claims that are made about benefits of that diet, and then to check whether the predicted benefits have materialized over the years; specifically, to see what government health data reveals about health outcomes that have occurred following the great increases in breastfeeding of children born since the early 1970's.  That kind of claim-by-claim consideration of the historical data for the period since the 1970's can be found at As it turns out, after examining the historical data regarding the disorders that Surgeon General Regina Benjamin alleges are reduced by breastfeeding, it is apparent that every disorder except one has instead actually increased since breastfeeding greatly increased.  Several of the disorders increased so much that they are now considered to be epidemics.


Mothers should not necessarily feel safe about their breast milk if they are rural non-smokers.  Whereas PAH's are apparently mainly taken in by inhalation, dioxins are mainly taken in by way of food; unless one lives in an unusually low-pollution food-source region, the only way to avoid typical concentrations of dioxins in breast milk is to adopt a basically vegetarian diet many years before breastfeeding starts.  Also, residential wood-burning emissions are a major source of BaP(50)  and particulate matter, and a significant source of lead, typically emitted in the immediate air supply of both lactating mothers and infants. Breast milk in rural Italian mothers was probably uniformly within acceptable limits of BaP at least partly because there is relatively little residential wood burning in sunny Italy, with minimal forests.  It is also important to bear in mind that backyard burning, often done in rural areas, has become the largest single source of releases of dioxins to the atmosphere in recent years, according to the EPA.  In addition, high levels of PBDEs in breast milk apparently result mainly from exposure of mothers to air around electronic devices. (See earlier in this section.)


One can be safe in assuming that most cows do not have nearly the exposure to diesel emissions, tobacco smoke, air surrounding electronic devices, and residential wood-burning pollution that human mothers have, not to mention not eating meat, fish and dairy products into which toxins have bio-accumulated.   




Section 2:   More on how these toxins harm development:

In addition to possible or known endocrine-disruption and sometimes potent mutagenic properties of PAHs,(51) many of the derivatives, also, "have been found to be highly mutagenic." (same EPA source, p. 2-90)  Mutagens should be of special concern because they can affect the descendants of a person who outwardly appears to be unaffected. Elsewhere in this paper there are various references to possible effects of environmental toxins on pregnant women and developing infants, and for brevity the possible effects on the genetic material in future parents of both genders will not be mentioned at the same time.  But it should be kept in mind that mutagens could be affecting genes of both men and women now in ways that may not be apparent in them but which could be expressed in their future children.



Section 2.a:  Effects of dioxins, PCBs and mercury in human milk:

Of interest is the study that was apparently the only one that has been carried out on the association between background exposure to POPs and clinically significant developmental disorders, such as learning disability or attention deficit disorder, among children from a general human population.  It utilized data for 278 children aged 12–15 who were included in the U.S. National Health and Nutrition Examination Survey 1999–2000.  The authors found dramatically increased odds of the children’s having these disorders if they had detectable levels of dioxins or furans. (Furans are chemical relatives of dioxins that are usually grouped together with dioxins.)   The average odds ratio of having Learning Disability for those with detectable levels of dioxins/furans, compared with those without detectable levels, was 2.33 (that is, a 133% increased likelihood); and the average odds ratio of having Attention Deficit Disorder for those with detectable levels of dioxins/furans, compared with those without detectable levels, was 3.02 (three times as likely).(51a)  Note that these effects were found not in a group of children with exceptionally high exposures, but in a group comprised of the (approximately) 30% of the population with the highest dioxin/furan concentrations.  This study should be seen in combination with findings by a two-researcher team headed by an EPA senior scientist (citing five other studies with compatible findings) indicating that six or more months of breast-feeding would result in accumulated dioxin exposure 6 times higher than that of a formula-fed infant during the first year of life; accumulated exposure was expected to still be twice as high among the breastfed children even after 10 years.(51b)  It should be safe to assume from this that by far the principal determinant of the extent of a developing child’s dioxin exposure and accumulation is breastfeeding.  And, as indicated by the study that was apparently the only one to assess effects of dioxin exposure on neurological development of older children in the general population (see above), increased dioxin exposure (at levels such as typically found in human milk) apparently can have serious effects.   It is especially of note that this study dealt with children old enough to give a reasonable indication of long-term effects of the toxins, as opposed to essentially all of the other studies assessing effects of such toxins, which tested children at much younger ages, before long-term effects would be so well demonstrated.


Since sex steroid hormones (especially testosterone) are known to be important to development of the brain (52), it is relevant to mention the following testosterone-reducing effects of dioxins:  According to a CDC report, dioxins have been demonstrated in animal studies to have effects including neurotoxicity, altered transcription of genes, altered thyroid function, and testicular atrophy.  According to researchers for the EPA, "In tests by at least two different research teams, dioxins were found to have effects on the male reproductive systems in rats tested, as follows: impaired testosterone synthesis, and possibly central nervous system sexual differentiation.(54)  It is worth repeating what was pointed out in the introduction, which is that the peak body-weight-based dose received by a breastfeeding infant is estimated in an EPA study to be 242 pg TEQ/kg-day.(4) This compares with the reasonably-safe upper threshold of dioxin exposure of 0.7 pg TEQ/kg-day estimated by the EPA.(3)  Also, note (with details and sources in Section 1.a of that exposure of infants to dioxins via breast milk is scores to hundreds of times higher than via formula.


A number of studies indicate that dioxins and dioxin-like compounds (which include some types of PCBs) decrease thyroid hormone levels, which are important to development of the brain.  According to the EPA's web page on health effects of PCBs, "Effects of PCBs on nervous system development have been studied in monkeys and a variety of other animal species. Newborn monkeys exposed to PCBs showed persistent and significant deficits in neurological development, including visual recognition, short-term memory and learning. Some of these studies were conducted using the types of PCBs most commonly found in human breast milk."(56)  According to an article in an industrial health journal, "Even low levels of dioxin or PCB exposure during the perinatal period can greatly influence neurological development" in this way and "can cause irreversible neurological damage."(57) 


To illustrate the potency of some of these developmental toxins, it is worth considering a test performed on rhesus monkeys with Aroclor 1248, a commonly-used commercial product that contained PCBs.  According to the U.S. ATSDR, Aroclors were “useful in a wide variety of applications, including dielectric fluids in transformers and capacitors, heat transfer fluids, and lubricants…. PCBs are combustible liquids, and the products of combustion may be more hazardous than the material itself.” (59)  Other common uses of PCBs included fluorescent light ballasts and plasticizers.(60)    “In rhesus monkey infants whose mothers were or had been exposed to Aroclor 1248 during gestation and lactation, behavioral testing showed hyperactivity and retarded learning ability….  These effects were reported at doses of about 0.006 mg Aroclor 1248/kg bw/day to the mothers.” (61)  Assuming a recognized average weight of 5.3 kg (12 pounds) per female monkey, this works out to 0.032 mg per monkey per day, or a dose of less than one 800,000th of one ounce of Aroclor per day per gestating/lactating female monkey.  Remember that, according to an expert study, “There is excellent correspondence between the effects of developmental PCB exposure in the monkey and that observed in humans, including learning deficits and changes in activity.”(15a)   


When considering the effects of 1/800,000th of an ounce of a PCB-containing product (see above), also bear in mind that 600,000 tons of PCBs were produced in the U.S. between 1930 and 1977, that they are very stable and are contained in considerable equipment that is still in use (and sometimes leaking); they are also heavily present in landfills, which are a major source of emissions of toxins to the atmosphere (especially during fires), not to mention the landfills’ drainage to water supplies.  Also bear in mind their persistence in the environment and their presence in diesel emissions,(58) which have been increasing rapidly in the U.S., according to the EPA's latest data.  In addition, indoor air in houses with floors finished with PCB-containing wood finish have been found to contain high levels of PCB. (62)  At the rate of wide use of a chemical for a half century or more before a finding that it is too toxic (as was the case with the pesticides endosulfan and dicofol), one may reasonably wonder about the safety of the materials that are now being used in place of PCBs, which could also end up being concentrated in human milk.  (Yes, most of the thousands of chemicals introduced into use in recent decades have not been tested for safety.) 

Fig. 3

The above chart is a German study's demonstration of the differences in concentrations of certain toxins found in infants who had been breastfed (the three “A” sections) compared with concentrations found in infants that had been bottle fed (the “B” sections), at 6 weeks and 6 months after birth.  (The specific toxins tested for here were DDEs and two variations of PCBs; DDE's are related to DDT, and the EPA has determined that both are probable human carcinogens.)(63)  The “B” sections show the much lower levels found in bottle-fed infants. The author of this 2006 study indicated skepticism as to whether the reported declines in certain toxins in the environment since the 1980's had actually resulted in significant reductions in possible harm to infants.


When observing (in the B sections above) how small the concentrations of toxins are in the bottle-fed infants, bear in mind that even those low concentrations shown include most of the toxins that were transferred to the fetus during gestation; most of the prenatal transfer is still stored in the infant’s body, since those toxins are of the “persistent” type.

Fig. 4 







This chart from a study published in 2014,(63a) like Figure 3 above, shows the dramatic increase in children’s PCB concentrations that is linked with breastfeeding.  This study found that hearing loss in the children was directly and very closely correlated with postnatal concentrations of PCBs, but it was not at all correlated with prenatal (maternal) concentrations.  Bear in mind that hearing acuity is fundamental to speech development, learning, much occupational effectiveness, social relationships, music appreciation and participation, and alertness to signs of danger; also be aware that at least one authoritative scientist believes that it is possible that delayed language development (which could result from hearing loss) could lead to traits of ASD.(63d)  


In the above study, OAEs, which are “an effective diagnostic tool for detecting hearing loss,” were measured in children with varying concentrations of PCBs; it was found that the difference between 75th percentile and 25th percentile (a very typical difference) in PCB concentrations was associated with a 1.6 decibel decrease in OAE amplitude. With that in mind, note that a 3 decibel decrease is the equivalent of reduction in sound power by 50%.(63b)  Judging by the magnitudes of the variations in PCB levels according to breastfeeding exposures, that kind of decrease appears to be in the range that is linked with extended breastfeeding as opposed to not breastfeeding.  Note in the above chart that the average difference in PCB concentrations between a non-breastfed child and an average child breastfed for 6 to 12 months was found to be about 850%.  This is compatible with information from studies such as shown in Figure 3 (above) and others.(63c)


Seeing (in the above two charts) how low the levels of toxins are in the bottle-fed infants as compared with the breastfed infants, even though those levels include most of the gestational transfer, this is a good demonstration of the results of the normal pattern described by experts on contaminants in breast milk, according to which "Significantly more (10 to 20 times) of a mother's body burden of persistent organohalogens is transferred to the infant via the milk than by the transplacental route."(64)  This should be seen in combination with the apparent fact that about 2½ times as much growth and development of the brain takes place during the year after birth as takes place prenatally. (see Figure 1 at


Some of the effects of mercury: 

“Mercury disrupts brain development by inhibiting important enzymes and preventing certain cells from dividing to produce more neurons and support cells (called glia). Research shows that mercury also increases the vulnerability of the brain to the adverse effects of other toxins at levels that are otherwise thought to be below dangerous thresholds.”(64a)  For other neuro-developmental  effects of mercury, see and



Section 2.a.1:  Exclusions and deletions of information that matters

Not every study of outcomes of postnatal exposure to toxins in breast milk has found negative outcomes.  But close reading of some of the studies that have failed to find negative outcomes reveals a good reason why they may well have overlooked important data.  In a 2006 Danish study (Debes et al.) of impact of mercury exposure “on neurobehavioral function” at age 14, the authors excluded 18 out of 878 exposed children from their study on the grounds that they had neurological disorders; and they then proceeded to find no adverse impact of postnatal mercury exposure on neurobehavioral function in the remaining children.(65)  It is very likely that they arrived at that finding because of their exclusion of 2% of the possible participants, those who were very likely to have been most affected by the exposure.  The above study was summarized in Myers et al., in a chart about developmental endpoints of postnatal mercury exposure, simply as follows:  “Postnatal exposure to methylmercury had no discernible effect.”(65a)  A reasonably accurate summary would have been, “Postnatal exposure to methylmercury had no discernible effect on those remaining after the researchers had excluded those who were very likely to have been most affected.”


Excluding participants or deleting relevant data from study findings, in ways that can substantially affect results, is apparently rather common. Doing a web search for “outliers in statistics” will reveal that it is typical -- or possibly even usual -- practice in studies to merely exclude outliers, those data points that don’t conform to the general pattern formed by the bulk of the findings.  The seemingly inconsequential percentages of the deleted cases (1-2%) are the numbers that apply to children with autism, which actually add up to many tens of thousands of individuals in the U.S.  The authors might or might not acknowledge that they had deleted outliers or excluded those participants who could well have been the ones whose outcomes would have revealed the worst effects of toxins.


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


At, there are listed over 50 studies that have found adverse health effects specifically associated with breastfeeding, or with more breastfeeding compared with less breastfeeding.  Those include the largest study ever conducted on the health effects of breastfeeding and the only one on effects of breastfeeding on obesity to have been randomized (the PROBIT study in Belarus), which is the recognized best way to avoid false conclusions resulting from confounders in studies. 


Section 2.b:   Pesticides, bromine and phthalates

Pesticides also, including some that are used residentially, have been widely found in breast milk.(66).  Section 1.6.a at provides details about connections between various pesticides to which fetuses and infants are exposed and (a) autism, (b) other changes in social behavior and brain development, (c) attention deficit disorders and hyperactivity disorders, (d) feminization of males and (e) masculinization of females.


Bromine is another neurological toxin excreted in breast milk; bear in mind that a mother could absorb bromine through her skin while in a pool or spa treated with bromine as a disinfectant.


Most of the research that has found developmental harm to result from exposure to these chemicals was based on tests with animals; but, according to a publication of Stanford University School of Medicine, “the chemical structures of hormones and their receptors are very similar among vertebrates, including humans. A chemical that binds with an estrogen receptor in mice is almost certainly going to bind with an estrogen receptor in people.”(67)   Research with human data has verified the results from animal tests regarding the testosterone-reducing, de-masculinizing effects of phthalates, another toxin known to be present in breast milk in higher concentrations than in alternative feedings. (Section 1.6.b at more information about phthalates, see Section 1.g of

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


Some commentators downplay the significance of the extraordinarily high dosage of toxins received by infants in breast milk, pointing out that, if one looks at that dosage spread out over a typical 70-year lifespan, it becomes a relatively minor addition to the typical total lifetime exposure to the toxins.  The problem with that viewpoint is that permanent, life-impairing neurological damage as well as childhood cancer can occur during infancy while effective exposure levels are many times higher than the later lifetime average, early levels that are especially high in relation to the infant's vulnerable stage of development.


As explained above, breast milk today is not the beneficial, safe substance today that it was in earlier times:  Essentially all of the toxins discussed above have begun to become major problems in the environment only beginning in the mid-20th-Century, with some of them (such as PBDEs, BPA and some pesticides) not becoming significant until very late in the 20th Century.  Many new types of pesticides were introduced only in the 1980's.(66)


For additional information about harm to neurological development that can result from lactational exposure to dioxins (remember that PCBs are a variation of dioxins), including a finding by a board of the National Academy of Sciences "suggesting that TCDD (dioxin) has the potential to disrupt a large number of critical developmental events...," see Section 2 of



Section 3:  Synergistic effects resulting from combined exposures to multiple toxins at low doses in breast milk

Developmental toxins have been discussed above one at a time, indicating harmful effects that have been found to apply to each toxin separately, because they have each been studied separately.  But there has been very little study of their combined effects.  What little study has been done of combined effects is not encouraging.  Low doses that are especially widespread in environments and in breast milk but which  by themselves don’t show up in studies as having harmful effects may have harmful effects when they interact with low doses of other environmental toxins known to typically be contained in breast milk.  Some sense of that can be gained merely by reading the titles of the following studies:

   a)  “Polybrominated diphenyl ethers, a group of brominated flame retardants, can interact with polychlorinated biphenyls in enhancing developmental neurobehavioral defects.”  Eriksson P, et al, Toxicol Sci. 2006 Dec;94(2):302-9. Epub 2006 Sep 15. at

   b)  “Low concentrations of the brominated flame retardants BDE-47 and BDE-99 induce synergistic oxidative stress-mediated neurotoxicity in human neuroblastoma cells.”  Tagliaferri S et al.,  2010 Feb;24(1):116-22. doi: 10.1016/j.tiv.2009.08.020. Epub 2009 Aug

   c) “Coexposure of neonatal mice to a flame retardant PBDE 99 (2,2',4,4',5-pentabromodiphenyl ether) and methyl mercury enhances developmental neurotoxic defects.”  Fischer C, et al., Toxicol Sci. 2008 Feb;101(2):275-85. Epub 2007 Nov 2. at

     And a related quote from another study:  “Of relevance is that while a low dose of each of these compounds did not produce any behavioral effect when given alone, upon co-exposure the same low doses of BDE-99 and PCB-52 produced significant behavioral alterations. These were equal, if not greater, than those caused by a high dose of each compound alone. (see “Overall perspective and research needs” section in reference (68))




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




Comments from readers:

From the inception of these publications in early 2012 until present, the invitation has been extended to all readers to submit criticisms, asking them to point out how anything written here is not well supported by authoritative sources (as cited) or is not logically based on the evidence presented.  As of February 1, 2014, after almost two years, only one specific comment about an inaccuracy in one of our articles has been received in response to that invitation.  (That is significant, considering the many thousands of visits we receive from readers every month.)  Our publications have been improved as a result of that criticism and also another comment indicating a different way of interpreting our research, and we look forward to receiving more comments.  To read those comments and our responses to them, as well as to read several other e-mails containing comments or questions and our responses to them, go to All comments are welcome, especially those that point out any deficiencies in our evidence in relation to conclusions drawn or any lack of quality in the reasoning as presented.  Please send comments, criticisms, or questions to . Quite clearly, many people don't like our conclusions; they just can't find anything wrong with the evidence or reasoning that leads to the conclusions.  Those who can't provide any criticisms of any of our content also include officials of government agencies that promote breastfeeding, who have received several letters from us, as well as the World Health Organization and the American physicians' associations that advocate breastfeeding.  The latter organizations haven't even responded to our letters (two to each organization) questioning them about the evidence on which they base their advocacy of breastfeeding.




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


(2). “More than 350 pollutants found in breast milk,”  Geoffrey Lean, Environment Correspondent  Sunday 11 July 1999  at  See also U.K. government document at   and “Call for action over polluted breast milk

Scientists highlight health risks as babies get 'cocktail of chemicals'”, Sue Quinn, The Guardian, Sunday 11 July 1999 20.44 EDT at


(2a)  See Section 1.c of .


(3) 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.”

(4) 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)


(5) 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.  Found at

Also: 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. doi: 10.1016/j.etap.2004.01.009. Abstract at

Also: 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

Also:  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. doi: 10.1016/j.envint.2011.03.022. Epub 2011 Apr 30. At

Also:  Li J, Zhang L, et al., A national survey of polychlorinated dioxins, furans (PCDD/Fs) and dioxin-like polychlorinated biphenyls (dl-PCBs) in human milk in China.  Chemosphere. 2009 May; 75(9):1236-42. doi: 10.1016/j.chemosphere.2009.01.073. Epub 2009 Feb 28.  At

Also:  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.chemosphere.2011.02.070. Epub 2011 Apr 6.   At

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


(6) 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.  Also see Sections 1.a, b and c of .


(7) See


(8) 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  The full text, including the quoted passages, can be purchased for $7 or reference librarians at local libraries could probably obtain it at no charge.  Other studies finding disproportionately high autism rates among more-breastfed children include the following:


Breastfeeding and Autism  P. G. Williams, MD, Pediatrics, University of Louisville, and L. L. Sears, MD, presented at International Meeting for Autism Research, May 22, 2010, Philadelphia Marriot, found at


Trends in Developmental, Behavioral and Somatic Factors by Diagnostic Sub-group in Pervasive Developmental Disorders: A Follow-up Analysis, pp. 10, 14   Paul Whiteley (Department of Pharmacy, Health & Well-being, Faculty of Applied Sciences, University of Sunderland, UK), et al.  Autism Insights 2009:1 3-17  at    Also:  Patterns of breastfeeding in a UK longitudinal cohort study, Pontin et al., School of Maternal and Child Health, University of West of England, Bristol, UK.  


(9) ATSDR  web page "Public Health Statement for DDT, DDE, and DDD,"September 2002, Section  at     The exact wording that was paraphrased here was, "The proper development of many systems and functions depends on the timely action of hormones, particularly sex steroids; therefore, interfering with such actions can lead to a wide array of effects that may include altered metabolic, sexual, immune, and neurobehavioral functions. Effects of this type, that occur following exposure during fetal life via the placenta or early in life caused by either direct exposure to chemicals or exposure via maternal milk, are discussed in this section."  

(11) at

(12)  Committee on Developmental Toxicology, Board on Environmental Studies and Toxicology, in Scientific Frontiers in Developmental Toxicology and Risk Assessment (2000) , Commission on Life Sciences,  The National Academies Press, p. 56


(12a)   Nagayama et al., Postnatal exposure to chlorinated dioxins and related chemicals on thyroid hormone status in Japanese breast-fed infants, Chemosphere. 1998 Oct-Nov;37(9-12)    


(12b)  U.S. EPA:  Toxicological Review of 2,2',4,4'-Tetrabromodiphenyl Ether (BDE-47)  EPA/635/R-07/005F, p. 40, at


(12c) Kodavanti, Neurotoxicity of Persistent Organic Pollutants: Possible Mode(s) of Action and Further Considerations,  Dose Response. 2005; 3(3): 273–305. Published online May 1, 2006.  p. 292 at


(13)  PCB-95 Modulates the Calcium-Dependent Signaling Pathway Responsible  for Activity-Dependent Dendritic Growth, Gary A. Wayman et al., Environmental Health Perspectives • volume 120 | number 7 | July 2012, found at


(14) 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


(15) Winneke G et al., PCB-related neurodevelopmental deficit may be transient: follow-up of a cohort at 6 years of age   Environ Toxicol Pharmacol. 2005 May;19(3):701-6. doi: 10.1016/j.etap.2004.12.040. Epub 2005 Jan 26.  found at


(15a)  Rice et al., Lessons for Neurotoxicology from Selected Model Compounds:

SGOMSEC Joint Report, Environ Health Perspect 1 04(Suppl 2):205-215 (1996), at


(15b) Seelbach et al., Polychlorinated Biphenyls Disrupt Blood–Brain Barrier Integrity and Promote Brain Metastasis Formation,  Environ Health Perspect. Apr 2010; 118(4): 479–484. Published online Oct 28, 2009. doi:  10.1289/ehp.0901334  at

Also  Selvakumar et al., Polychlorinated biphenyls impair blood-brain barrier integrity via disruption of tight junction proteins in cerebrum, cerebellum and hippocampus of female Wistar rats: neuropotential role of quercetin, Hum Exp Toxicol. 2013 Jul;32(7):706-20. doi: 10.1177/0960327112464798. Epub 2012 Nov 15.  at


(15c) Polanska et al., Review of current evidence on the impact of pesticides, polychlorinated biphenyls and selected metals on attention deficit / hyperactivity disorder in children, Int J Occup Med Environ Health. 2013 Mar;26(1):16-38. doi: 10.2478/s13382-013-0073-7. Epub 2013 Mar 22.  at


(16) "Environmental toxicants and the developing immune system: a missing link in the global battle against infectious disease?"  Bethany Winans, et al., Reprod Toxicol. 2011 April; 31(3): 327–336. Published online 2010 September 22. doi: 10.1016/j.reprotox.2010.09.004  PMCID: PMC3033466  NIHMSID: NIHMS245165  accessed at  citing the following:


 Heilmann C, Grandjean P, Weihe P, Nielsen F, Budtz-Jorgensen E. "Reduced antibody responses to vaccinations in children exposed to polychlorinated biphenyls." PLoS Med. 2006;3:e311. [PMC free article


   Weisglas-Kuperus N, Patandin S, Berbers GA, Sas TC, Mulder PG, Sauer PJ, et al. "Immunologic effects of background exposure to polychlorinated biphenyls and dioxins in Dutch preschool children." Environmental health perspectives. 2000;108:1203. [PMC free article]


   Glynn A, Thuvander A, Aune M, Johannisson A, Darnerud P, Ronquist G, et al. "Immune cell counts and risks of respiratory infections among infants exposed pre- and postnatally to organochlorine compounds: a prospective study". Environmental Health. 2008;7:62. [PMC free article]


   Dallaire F, Dewailly E, Muckle G, Vezina C, Jacobson SW, Jacobson JL, et al. "Acute infections and environmental exposure to organochlorines in Inuit infants from Nunavik." Environ Health Perspect. 2004;112:1359–63. [PMC free article]


   Dewailly E, Ayotte P, Bruneau S, Gingras S, Belles-Isles M, Roy R. "Susceptibility to infections and immune status in Inuit infants exposed to organochlorines.” Environ Health Perspect. 2000;108:205–11. [PMC free article]


    Jedrychowski W, Galas A, Pac A, Flak E, Camman D, Rauh V, et al. "Prenatal ambient air exposure to polycyclic aromatic hydrocarbons and the occurrence of respiratory symptoms over the first year of life." European journal of epidemiology. 2005;20:775–82.


    Weisglas-Kuperus N, Vreugdenhil HJ, Mulder PG.  "Immunological effects of environmental exposure to polychlorinated biphenyls and dioxins in Dutch school children." Toxicol Lett. 2004;149:281–5.


    Guo YL, Lambert GH, Hsu CC, Hsu MM. Yucheng: "Health effects of prenatal exposure to polychlorinated biphenyls and dibenzofurans." Int Arch Occup Environ Health. 2004;77:153–8.


    Vos JG, Moore JA. "Suppression of cellular immunity in rats and mice by maternal treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin." International archives of allergy and applied immunology.


Also:   Potential for early-life immune insult including developmental immunitoxicity in autism and autism spectrum disorders:  Focus on critical windows of immune vulnerability  Dietert and Dietert, Journal of Toxicology and Environmental Health, PartB, 11:600-680, 2008  Taylor and Francis Group, LLC


(17) 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 in 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.


(20) Neurotoxicology.  2007 November; 28(6): 1047–1067. Published online 2007 August 24.  PMCID: PMC2118052 NIHMSID: NIHMS34875  Developmental Neurotoxicity Of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Lucio G. Costa et al. at


(21)  Polybrominated Diphenyl Ethers (PBDEs) in Breast Milk and Neuropsychological Development in Infants   US National Library of Medicine National Institutes of Health  Environ Health Perspect  v.120(12); Dec 2012 > PMC3548276   Environ Health Perspect. 2012 December; 120(12): 1760–1765.  at


(23) Shokuhin Eiseigaku Zasshi. 2004 Aug;45(4):175-83. PubMed – NCBI   Polybrominated diphenyl ether flame retardants in foodstuffs and human milk. Akutsu K, Hori S.  Osaka Prefectural Institute of Public Health: 1-3-69, Nakamichi,Osaka 537-0025, Japan


(23a) ”Steroid Hormones and Brain Development: Some Guidelines for Understanding Actions of Pseudohormones and Other Toxic Agents" by Bruce S. McEwen, Laboratory of Neuroendocrinology, Rockefeller University, New York, NY (published in Environmental Health Perspectives Vol. 74, pp. 177-184, 1987).


(23b) de Cock et al., Does perinatal exposure to endocrine disruptors induce autism spectrum

and attention deficit hyperactivity disorders? Review, Acta Pediatrica 2012, at


(24) 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: PMC3491946  at


(25)  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]  Gascon M et al.

(26)  Branchi et al., Polybrominated diphenyl ethers: neurobehavioral effects following developmental exposure. Neurotoxicology. 2003 Jun;24(3):449-62.  at


(26a) Eskenazi et al., In Utero and Childhood Polybrominated Diphenyl Ether (PBDE) Exposures and Neurodevelopment in the CHAMACOS Study, Environ Health Perspect; 2013, DOI:10.1289/ehp.1205597 at


(27)  Mini-review:  Polybrominated diphenyl either (PBDE) flame retardants as potential autism risk factors  Anne Messer,  2010 Elsevier   Physiology and Behavior  100 (2010)  245-249    at;   for additional evidence of causal effect of PBDEs on ADHD-like behavior:   In utero and childhood polybrominated diphenyl ether (PBDE) exposures and neurodevelopment in the CHAMACOS study  Eskenazi B et al.,  Environ Health Perspect. 2013 Feb;121(2):257-62. doi: 10.1289/ehp.1205597. Epub 2012 Nov 7.

(27a) Eskenazi et al. 2013. In Utero and Childhood Polybrominated Diphenyl Ether (PBDE) Exposures and Neurodevelopment in the CHAMACOS Study. Environmental Health Perspectives 121(2):257-262. at  referred to in Chen et al., below (27d)


(27b) Giordano et al., Developmental Neurotoxicity: Some Old and New Issues, ISRN Toxicol. 2012; 2012: 814795, PMCID: PMC3658697 at as quoted in, Section1.b.

(27b1) See Section 1.b of, especially sources cited in footnote #25.

(27b2)  (Chang et al., Autism and Sensory Processing Disorders: Shared White Matter Disruption in Sensory Pathways but Divergent Connectivity in Social-Emotional Pathways, Plos One, July 2014, at

(27b3) Tau et al., Normal Development of Brain Circuits, Neuropsychopharmacology. Jan 2010; 35(1): 147–168. Published online Sep 30, 2009   at

(27b4)  Life Sciences Learning Center, University of Rochester:  Brain Development and Toxins, 2013, at

(27b5)  National Scientific Council on the Developing Child, Early Exposure to Toxic Substances Damages Brain Architecture, 2006, p. 3, at

(27b6)  P. Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants,  Environmental Health Perspectives, accepted Oct. 1993

(27b7) Exploration Of Perinatal Pharmacokinetic Issues  Contract No. 68-C-99-238, Task Order No. 13  Prepared for:  Office of Research and Development,  U.S. Environmental Protection Agency  Prepared by:  Versar, Inc.  EPA/630/R-01/004   Section,  at


(27b8) 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, the increase in the infants’ mercury levels attributable to breastfeeding was probably well over 200% during the first 6 months of breastfeeding.

(27b9) Yang et al., Developmental Exposure to Polychlorinated Biphenyls Interferes with Experience-Dependent Dendritic Plasticity and Ryanodine Receptor Expression in Weanling Rats, Environ Health Perspect;, March 2009,  DOI:10.1289/ehp.11771 at

(27b10) de Cock et al., Does perinatal exposure to endocrine disruptors induce autism spectrum and attention deficit hyperactivity disorders? Review, Acta Pediatrica 2012, at 


(27b11)  PBDEs in infant formula, detected at 32 and 25 pg/g wet weight:  p. 4-77, 2nd paragraph of Section 4.7 (citing Schechter et al.) 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


PBDEs ingested by breastfed infants, 1,056 pg/g wet weight:  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, 4th paragraph from end,  at


(27c) Herbstman et al. 2010. Prenatal Exposure to PBDEs and Neurodevelopment. Environ Health Perspect 118(5):712-719  at; referred to in Chen et al., below.


(27d) Chen et al., Prenatal Polybrominated Diphenyl Ether Exposures and Neurodevelopment in U.S. Children through 5 Years of Age: The HOME Study,  in Environmental Health Perspectives, May 2014, at    “A ten-fold increase in prenatal BDE-47 was associated with a 4.5-point decrease (95% CI: -8.8, -0.1) in Full Scale IQ and a 3.3-point increase (95% CI: 0.3, 6.3) in the hyperactivity score at age 5 years.”

(28)  National Academies of Science report on dioxins in the food supply.

(30) Schecter, A., et al. Chlorinated Dioxins and Dibenzofurans in Human Tissue from General Populations: A Selective Review, Environmental Health Perspectives Supplements 1994; 102(Supple 1): p. 159-171  and  Schecter, A., et al. Congener-specific Levels of Dioxins and Dibenzofurans in U.S. Food and Estimated Daily Toxic Eequivalent Intake, Environmental Health Perspectives Journal 1994; 102(11): p. 962-966.

(31). Regulatory Toxicology and Pharmacology, 37 (2003) 202 217 Dioxin risks in perspective: past, present, and future  Hays and  Aylward  at


(32) Verbreitung, Dauer und zeitlicher Trend des Stilles in Deutschland, Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz. 2007 May-Jun;50(5-6), p. 624



(34). "Paying a Price for Loving Red Meat" in Personal Health, by Jane E Brody, New York Times: April 27, 2009

(35)  National Academies of Science report on dioxins in the food supply.

(36). EPA-452/R-97-006, December 1997, Table 2-3

(37).   p. 28 of UNEP Global Mercury Assessment 2013 at

(37a) National Scientific Council on the Developing Child, Early Exposure to Toxic Substances

Damages Brain Architecture, 2006, at


(38).   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  Executive Summary, p. xxiii

(39)Brominated Flame Retardants, Third annual report to the Maine Legislature, Jan. 2007, Maine Dept. of Environmental Protection, Maine Center for Disease Control and Prevention, Dr. Deborah Rice et al.

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


(41). Table 3 of Developmental Neurotoxicity of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Costa et al., Neurotoxicology. 2007 November; 28(6):   NIHMS34875 at  

(41a)  Fürst P., Dioxins, polychlorinated biphenyls and other organohalogen compounds in human milk. Levels, correlations, trends and exposure through breastfeeding.  Mol Nutr Food Res. 2006 Oct;50(10):922-33.

(42) ToxTown of National Library of Medicine, at




(44)  Transfer of Polycyclic Aromatic Hydrocarbons to Fetuses and Breast Milk of Rats Exposed to Diesel Exhaust, Tozuka, Watanabe et al., Kanazawa University and Tokyo Metropolitan Public Health Research Institute; Journal of Health Science 50(5) 2004 pp. 497-502

(45) Chemosphere. 2007 Apr;67(7):1265-74. Epub 2007 Jan 26.  Polycyclic aromatic hydrocarbons (PAHs) in human milk from Italian women: influence of cigarette smoking and residential area.  Zanieri L, et al., University of Florence, Department of Chemistry,  Florence, Italy. At




(47).   "Residential Proximity to Freeways and Autism in the CHARGE Study" , Environmental Health Perspectives, Published in 119(6) Jun 2011, Heather E. Volk, Irva Hertz-Picciotto et al., reported (with doubling comment) in ScienceDaily (Dec. 17, 2010), "Proximity to Freeway Associated With Autism"

(48). Figure 1-8 in EPA/600/P-03/002F November 2006 An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000


(49). 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




(51) EPA/600/8-90/057F  May 2002, Health Assessment Document for Diesel Engine Exhaust, Table 2-22.  National Center for Environmental Assessment, Office of Research and Development, EPA


(51a) 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


(51b) Lorber et al.,  Infant Exposure to Dioxin-like Compounds in Breast Milk, Volume 110 | Number 6 | June 2002 • Environmental Health Perspectives (a peer-reviewed journal published by the National Institute of Environmental Health Sciences of NIH)


(52) Sex matters in autism and other developmental disabilities, Thompson, Caruso and  Nellerbeck, Journal of Learning Disabilities, Sage Publications, London, Thousand Oaks and New Delhi  p. 352, referring to COLLAER, M. L. & HINES, M.  ‘Human Behavioral Sex Differences: A Role for Gonadal Hormones during Early Development?’, Psychological Bulletin. 

Also Auyeung et al., Prenatal and postnatal hormone effects on the human brain and cognition, Pflugers Arch - Eur J Physiol, 2013, at   These authors cite five other studies in support of their generalization that experiments with a wide range of mammals “consistently” support the importance of testosterone to development of the brain.


(54) Stephen B. Klein and B. Michael Thorne in their Biological Psychology (2006), Worth Publishers, p. 390


(56) EPA web page on health effects of PCBs at


(57) Industrial Health 2000, 38, 259–268 Review Article:  The Effects of Dioxin on Reproduction and Development  Junzo YONEMOTO  National Institute for Environmental Studies, Japan  p. 262; at 

Also Glorieux et al., 1988; Rovet et al., 1987; Haddow et al., 1999)." (Prioritization of Toxic Air Contaminants  -- Children's Environmental Health Protection Act (State of California), October, 2001


(58)  C.A. Laroo et al., Emissions of PCDD/Fs, PCBs and PAHs from a Modern Diesel Engine Equipped with Catalyzed Emission Control Systerms, Environmental Science and technology, ACS Publications, June 30, 2011


(59) from the  ATSDR website page on Aroclors




(61) 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.


(62). Environ Health. 2008; 7: 2. Published online 2008 January 17. doi: 10.1186/1476-069X-7-2  Rudel et al; licensee BioMed Central Ltd.  PCB-containing wood floor finish is a likely source of elevated PCBs in residents' blood, household air and dust: a case study of exposure


(63) Gerd-Michael Lackmann,   Human Milk, Environmental Toxins and Pollution of Our Infants: Disturbing Findings during the First Six Months of Life   Int J Biomed Sci. 2006 June; 2(2): 178–183. PMCID: PMC3614598  found at


(63a) Jusko et al.,  Prenatal and Postnatal Serum PCB Concentrations and Cochlear Function in Children at 45 Months of Age, Environmental Health Perspectives, 22 July 2014 (Advance Pub.) at


(63b) dB: What is a decibel? at


(63c) see Section 1.a of 


(63d) Dr. Meng-Chuan Lai, of England’s Cambridge Autism Research Centre, quoted in “Language Delay Leaves Signature in Brains of Adults with Autism” - at


(64).  Jensen, A.A. et al, Chemical Contaminants in Human Milk, CRC Press, Inc., Boca Raton, Ann Arbor, Boston, 1991,  p 15.   Findings of above confirmed in animal tests, with even greater contrasts, in Ahlborg et al., Risk Assessment of Polychlorinated Biphenyls (PCBs), Nordic Council of Ministers, Copenhagen.  Report NORD 1992; 26 


(64a) National Scientific Council on the Developing Child, Early Exposure to Toxic Substances

Damages Brain Architecture, 2006, pages 7 and 9, at


 (65).  Debes F et al., Impact of prenatal methylmercury exposure . Neurotoxicol Teratol. 2006 May-Jun;28(3):363-75. Epub 2006 May 24

(65a) Gary J. Myers et al., Postnatal Exposure to Methyl Mercury from Fish Consumption: a Review and New Data from the Seychelles Child Development Study, Neurotoxicology. 2009 May; 30(3): 338–349. Published online 2009 January 21. doi:  10.1016/j.neuro.2009.01.005  PMCID: PMC2743883  NIHMSID: NIHMS119840  at 

(66). Environmental Health Perspectives, Vol. 109, No.1, Jan. 2001

(67). Challenged Conceptions: Environmental Chemicals And Fertility" 2005, a publication of Stanford University School of Medicine, p. 10

(68)   Neurotoxicology.  2007 November; 28(6): 1047–1067. Published online 2007 August 24.  PMCID: PMC2118052 NIHMSID: NIHMS34875  Developmental Neurotoxicity Of Polybrominated Diphenyl Ether (Pbde) Flame Retardants, Lucio G. Costa et al.  at

 Source of Figure 5. Maria Malgorzata Ulaszewskaa et al., PCDD/Fs and dioxin-like PCBs in human milk and estimation of infants’ daily intake: A review    Chemosphere   Volume 83, Issue 6, April 2011, Pages 774–782  at  



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 As indicated in the charts below, the postnatal period is one of especially rapid development of the brain and therefore special vulnerability to developmental toxins.

According to a 2009-2010 study with more updated data in this field in which more is being learned regularly, “During the early postnatal period…  cortical neurogenesis and neuronal migration continue through the postnatal period (Bhardwaj et al, 2006; Shankle et al, 1999)….  Thus, perinatal and early postnatal brain development features the onset of myelination and a striking development of gray matter connections, especially in sensorimotor and visual cortices.  (Tau et al., Normal Development of Brain Circuits, Neuropsychopharmacology. Jan 2010; 35(1): 147–168. Published online Sep 30, 2009   at


Other sources:

B.S. McEwen, Steroid Hormones and Brain Development: Some Guidelines for Understanding Actions of Pseudohormones and Other Toxic Agents, (Environmental Health Perspectives Vol. 74, pp. 177-184, 1987).  Research in the author's laboratory was supported by NIH Grant NS07080 and NIMH Grant MH41256.   “…the developing brain is an important target organ for the action of steroid hormones.Neural sensitivity to adrenal and gonadal hormones begins

during embryonic life, and during the period of early development the nervous system responds to hormones by altering cell proliferation, neuronal growth,and differentiation.”

(2g)  Gennaro Giordano and Lucio G. Costa1 , Developmental Neurotoxicity: Some Old and New Issues ISRN Toxicol. 2012; 2012: 814795. Published online 2012 June 24. doi: 10.5402/2012/814795  PMCID: PMC3658697

0(6b)  Prenatal exposure to organic halogens, including brominated flame retardants, influences motor, behavioral and cognitive performance at school age.  Environmental Health Perspect. 2009:117:1953-8  Roze E. et al.

0(8)  ATDSR document on dioxins, section on environmental sources      

 (26b)  Assessment of Benzo(a)pyrene Emissions in the Great Lakes Region at

0(91). CAS No: 7726-95-6)  Health-based Reassessment of Administrative Occupational Exposure Limits,  Committee on Updating of Occupational Exposure Limits, a committee of the Health Council of the Netherlands

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