Emissions from Waste Incinerators and Coal-fired Power Plants in Relation to Geographic Differences in Prevalence of Autism in the U.S.
Section 1, intro: Outstandingly high and low prevalences of autism in different parts of the U.S. are associated with presence or scarcity of waste incinerators:
Autism prevalence in three parts of the U.S. (as found in a recent study) is associated with pollution as follows:
a) mercury pollution and autism are both lowest in the Southeast, and
b) mercury from waste incineration and autism are both highest in two separate areas: Indiana and New England.
Complete text and sources at Section 1.
Section 2, intro: Other evidence linking mercury and/or other pollutants with autism:
At least ten published studies have found high levels of mercury in those with ASD. According to the EPA, “There is general agreement that the nervous system continues development in post-natal life and that methylmercury can adversely affect the developmental processes.” 90 Complete text and sources at Section 2.
Section 3, intro: Reasons why waste incinerators in the area may make a major difference in autism prevalence:
In addition to mercury, waste incineration is also known to emit substantial dioxins. Municipal waste incineration is the largest source of dioxins to the air in the U.S. PCBs and PBDEs would also normally be included in those emissions. Complete text and sources at Section 3.
Section 4, summary: Long-term harmful effects of dioxins, PCBs and PBDEs:
"Early developmental exposures to these chemicals are particularly devastating,” according to a toxicology textbook. A 2014 study found an increase in social problems, thought problems and aggressive behavior in relation to increasing postnatal background dioxin exposure. In another study, in line with the sex ratio in autism diagnoses, boys with elevated dioxin exposure, but not girls with such exposure, were found to have decreased expressive communication scores. A 2007 study found that learning disability and attention deficit disorder were two and three times as high among children with elevated levels of dioxins, compared with children with undetectable dioxin levels.
PBDEs, also, have been found to be high in incinerator emissions, at up to 1000 times higher than in typical U.S. ambient air samples. The EPA says that PBDEs have “adverse neurobehavioral effects following exposure during the postnatal period," and the EPA also sees neurobehavioral effects of PBDE exposures as being a “critical endpoint of concern.”
For the complete text, together with citations of sources, go to Section 4.
Section 5, summary: A study that specifically implicated waste incineration in traits of autism:
A very large 2013 study in Taiwan concluded that, of the different sources of environmental pollution investigated, the presence of an incinerator was the only one that affected parent-perceived child development directly. Among a major group of children, in the population residing within three kilometers from the incinerators, adverse neurodevelopmental effects were found.
Complete text and sources at Section 5.
Section 6, summary: One specific population group showed outstandingly high effects of the exposures to incinerator emissions:
Among children in the general population living within three kilometers of the incinerators, only minor effects of the emissions were found. But among children who lived near an incinerator and were breastfed, there were signs of increased risk of traits of ASD, ADHD and other developmental delays. Dioxin exposures via breastfeeding were implicated, according to the authors.
Dioxins, mercury, PBDEs, and PCBs are all developmental toxins, which become concentrated in human milk. Although dioxins have reportedly been declining in environments for decades, that chemical has since 2000 been found to be present in human milk in concentrations scores to hundreds of times higher than the relatively safe reference dose established by the EPA and at over 100 times the concentration in infant formula.
There are apparent connections, indicated by studies, between long-term intakes of dioxins by fully-grown bodies, transfers of the accumulated toxins to developing infants via lactation, and neurological effects in those infants. Other neurodevelopmental toxins in incinerator emissions (PBDEs, PCBs and mercury) also accumulate in maternal fat and are also transferred in breast milk. The postnatal period, like the prenatal period, is a period of vulnerability to effects of developmental toxins, according to the highest authorities; according to the EPA, neurological vulnerability is greatest after birth to PBDEs, which dramatically increased in industrialized environments in the late 20th century.
Complete text and sources at Section 6.
Section 7, summary: Something else could also be contributing to the major regional differences in autism prevalence:
According to data from the CDC, the twelve states of the U.S. Southeast, where autism is 50% below the U.S. average, have a mean 12-month duration of breastfeeding rate that is one third below the national average. In addition, unusually low exclusiveness of breastfeeding in that region could account for limitation of transfers of developmental toxins to infants. Complete text and sources at Section 7.
Section 8, Summary: Other evidence linking early-life exposures in the U.S. to autism according to location
Section 1: Outstandingly high and low prevalences of autism in different parts of the U.S. associated with presence or absence of waste incinerators:
A U.S. study published in 2017 (Hoffman et al.1) investigated associations between residential location and ASD in the children of Nurses' Health Study II women, including 486 with ASD. Children born in New England were found to be 50% more likely to be diagnosed with ASD compared to the average for children born in the US, and children in the Southeast were found to be half as likely to have ASD, compared with the average; in addition, an area consisting basically of the state of Indiana was found to have an unusually concentrated prevalence of autism. The authors reported that "patterns were not explained by geographic variation in maternal age, birth year, child's sex, community income or prenatal exposure to hazardous air pollutants, indicating that spatial variation is not attributable to these factors."
This map, from a 2007 report published by the U.S. National Oceanographic and Atmospheric Administration, shows major "point sources" (large, concentrated sources) of mercury in the U.S. -- omitting here the western U.S., which has relatively little of this pollution.2
Note the yellow ellipses surrounding Indiana (on the left) and New England (at the upper right; the thinly-populated far-northern part of New England is outside the marked area.) Observe the extraordinarily large proportions of both of these areas that are comprised of blue symbols, indicating emissions from waste incineration. To be precise, a few of the blue symbols in the area marked for New England are just outside the borders of that region, on the western and southern edges of the area; but considering the northward and eastward directions in which the prevailing winds blow in this general area,3 much or most of the emissions from incinerators in those adjacent areas would travel into New England.
In addition, note the lower presence of those pollution sources in the U.S. Southeast, which is basically the bottom half of the map.
So the reader's attention might be caught by the associations between pollutant sources and autism prevalence in three parts of the U.S. that are shown on this map:
a) autism and mercury from waste incineration are both highest in two distinct, separate areas: Indiana and New England; and
b) mercury pollution point sources and autism are both lowest in the Southeast.
Section 2: Evidence linking mercury and/or other pollutants with autism:
At least ten published studies have found high levels of mercury in those with ASD.4
A publication of Harvard University’s Center on the Developing Child, when discussing “prenatal and early childhood exposures to substances that have clearly documented toxic effects on the immature brain,” mentions only three leading examples of such neurodevelopmental toxins, one of which is mercury.5 The authors gave mercury in fish as a specific example of a source of toxins of concern, indicating that exposures expected to cause neurological harm can consist merely of rather common exposures. It is worth emphasizing here the reference by this authoritative source to "early childhood" as a time when exposures to mercury can have toxic effects on the immature brain; there is a widespread notion that postnatal exposures to developmental toxins do not have serious effects, but this group clearly rejects that idea.
Ethylmercury, as has often been used in vaccines, has been widely vindicated as being a cause of autism; but ethylmercury is only one of a number of species of mercury, and several other forms are authoritatively recognized to be neurological toxins. Methylmercury is listed by the International Program of Chemical Safety as one of the six most dangerous chemicals in the world's environment.6 Data from a major U.S. government survey indicates that methylmercury comprises about 82% to 94% of the mercury in women whose mercury levels are in the top quarter.7 Methylmercury is efficiently absorbed by most infants,8 and it accumulates in the brain. 6 According to the EPA, “There is general agreement that the nervous system continues development in post-natal life and that methylmercury can adversely affect the developmental processes.”9
According to both a national survey10 and a 2011 study reporting research by health departments of three states, about 8% of U.S. infants at birth already have mercury levels exceeding the EPA’s relatively-safe Reference Dose.11 It is very likely that there would be even higher exposures among infants and children downwind from the mercury sources (including waste incinerators) shown in the above chart.
Section 3: Why should waste incinerators in the area make a big difference in autism prevalence?
In addition to mercury, waste incineration is also known to emit substantial dioxins. The chemical designations for the two major types of dioxins are PCDD and PCDF, which is how they are referred to in the chart below.
Municipal waste incineration is shown to be the largest source of dioxins to the air in the U.S., and medical waste incineration is the second largest.
Notice the use of a "log scale" on the horizontal axis of this chart, which means that municipal waste incineration alone is shown to emit several times as much dioxin as coal combustion, at the middles of their estimated ranges as shown here.
Other toxins contained in waste incineration emissions are not as well studied, but notice (at the bottom of the chart) the authors' statement that PCBs would normally also be included in those emissions, and in the next section read about PBDEs also in those emissions.
So we need to consider what is known about neurodevelopmental effects of the other major toxins contained in incinerator emissions.
Section 4: Long-term harmful effects of dioxins, PCBs and PBDEs:
Dioxins and PCBs:
A major toxicology textbook published in 2011, with 21 contributing authors, states as follows regarding developmental effects of dioxins and PCBs: “These studies have indicated that … the most susceptible period of exposure is during development..," including in the postnatal period. Also, “early developmental exposures to these chemicals are particularly devastating.” (p. 551, bottom)12
One effect of dioxins and PCBs, which has been verified in animal experiments, is reduction of testosterone production in males.13 In addition to its role in reproduction, testosterone is also important to neurological development. Experts on neurological development point out that testosterone "clearly affects brain development;" they refer to the "critical period for the testosterone organizational effect" that takes place when the brain is developing.14
A study published in 2014, investigating developmental effects of dioxins in the Netherlands, where background levels were at levels that the authors described as "similar" to what was found in other industrialized countries, found the following in boys at ages 8 to 12: "an increase in social problems (p<0.001), thought problems (p=0.005), and aggressive behaviour (p=0.001)," as reported by teachers, in relation to increasing postnatal background dioxin exposure.15 Bear in mind that problems in social interaction are a core characteristic of ASD, and the other two problem areas mentioned above are often found in those with ASD. (The p values shown all indicate very high levels of statistical significance.) The relevant infant exposures took place in about 1990, decades past the peak level of dioxins in many industrialized environments.
The authors commented that "It is alarming to find a significant increase in aggressive behaviour and social problems ... in relation to background dioxin concentrations... both the teachers and parents reported abnormalities.... Furthermore, there is (scientific) literature evidence to support these findings of neurodevelopmental toxicity."
Boys with elevated dioxin exposure, but not girls with such exposure, were found in a study to have decreased expressive communication scores.16 Remember the 4.5-to-1 male-to-female ratio of autism, a disorder in which impaired communication is a core trait.
A 2007 study by an international research team (Lee et al.) tested children at ages 12 and 15, thereby permitting good indications of long-term effects of developmental toxins. This study found that learning disability and attention deficit disorder were two and three times as high among children with elevated levels of dioxins, compared with children with undetectable dioxin levels.17 The dioxins associated with such dramatic increases in risk of neurological disorders were at common background levels -- found in 27% to 31% of children. And the concentrations measured were clearly, basically from postnatal exposures, at those ages. Bear in mind that learning disability and attention deficits are common among people with ASD.
PBDEs, also, have been found to be high in incinerator emissions, at up to three orders of magnitude (very roughly, 1000 times) higher than in typical U.S. ambient air samples.18 According to the U.S. Agency for Toxic Substances and Disease Registry (ATSDR), “results from human studies are suggestive of an effect of PBDEs on neurodevelopment in children, including impaired cognitive development (comprehension, memory), impaired motor skills, increased impulsivity, and decreased attention.”19 Whereas the ATSDR indicates probability above, a statement by the EPA shows nothing but certainty regarding PBDEs' “adverse neurobehavioral effects following exposure during the postnatal period." And the EPA clearly sees those effects as being serious; they refer to neurobehavioral effects of PBDE exposures as being a “critical endpoint of concern.”20
Given the above, there is ample reason to see a possible causal connection between waste incineration, with its recognized emissions of dioxins, mercury and PBDEs (and probably PCBs), and increased prevalence of ASD. This should be considered as a possible explanation for existence of various geographic areas of elevated and reduced prevalence of ASD, as found in the recent study. As indicated in Figure 1 and accompanying text, higher and lower levels of autism in the U.S. appear to align well with higher and lower levels of major mercury emissions, but especially with emissions from waste incinerators with their additional toxic contents as discussed above.
Section 5: A study that specifically implicated waste incineration with observation of traits of developmental disorders:
A 2013 study in Taiwan (Lung et al.21), by researchers who collectively are authors or co-authors of many hundreds of studies and articles,21a worked with data from over 21,000 children, 953 of whom lived within three kilometers of a municipal incinerator. They concluded that "the results from our large-scale national birth cohort study show that, of the different sources of environmental pollution investigated, the presence of an incinerator was the only one that affected parent-perceived child development directly." (They cited other studies as having found parental observations to be valid.) Adverse effects associated with the local incinerator on neurodevelopmental outcomes were reported among a major group of children, in the population residing within three kilometers from the incinerators.
So there appears to be reason based on this study to consider proximity to waste incinerators to be related to possible causal factors for autism. In attempting to explain their findings, the authors referred to dioxins, PCBs and mercury as having been found to be significantly present in incinerator emissions. This aligns with our discussion in Section 4, about possible explanations for why autism was unusually high in the areas of waste incineration on the map of the eastern U.S.
Section 6.a: One specific population group showed outstandingly high effects of the exposures to incinerator emissions:
The authors of the above study conducted a comparison of development of children according to different possible risk factors. Among children in the general population living within three kilometers of the incinerators, the effects appeared to be relatively minor.
But the study reported that "those children who lived near an incinerator and were breastfed had an increased risk of U/DDD." (U/DDD was said to include developmental delay, ASD, and ADHD) As a proposed explanation for this finding, the authors said that "toxins can be transmitted via breastfeeding by mothers who are exposed;" more specifically, the authors said that "previous studies have found that milk from women who live near incinerators contains traces of dioxins...." They reported that breastfeeding was indirectly associated with negative neurodevelopmental outcomes in both of two separate types of analysis that they carried out.
The authors carefully distinguished between direct associations with incinerator proximity and indirect effects, the latter being those that were mediated by breastfeeding. They reported that "up to the age of 36 months, no direct association was found between living near an incinerator and the parents’ perception of the level of development of the children in the cohort;" and the only association found at that final (36 month) time point was with gross motor development. But it was very different with regard to the indirect effects, which related neurodevelopmental problems positively with proximity to incinerators among children who had been breastfed (as quoted above).
Section 6.b: Summarizing what was observed in the above study:
1) The general finding, when looking at the complete population, was that proximity to an incinerator was associated with U/DDD (which includes autism): "More parents who lived near an incinerator reported concerns that their children had mild or moderate U/DDD at 18 months, as compared with those who did not live near an incinerator."
But when the parent/child populations were investigated separately according to whether the children were breastfed at six months or not,
2) "an indirect effect was found with respect to the presence of an incinerator on U/DDD through the mediator of breastfeeding."
But on the other hand, when the indirect effect of breastfeeding was removed from the picture,
3) "no direct association was found between living near an incinerator and the parents’ perception of the level of development of the children in the cohort."
So there appears to be good evidence suggesting that exposures to pollutants from waste incinerators may have harmful effects on development if those toxins are ingested by infants indirectly via breastfeeding, but not when the toxins are only inhaled directly.
Although seemingly counter-intuitive, such a pattern is fully in line with what is known about the slow absorption by inhalation of certain toxins taken in over the long-term and accumulated (see Section 6.d as well as "slow accumulation..." below) and concentrated. Later they can be rapidly excreted to infants during the process of lactation. That process will be discussed below.
(As an aside, consider how this might relate to the apparent correlation of higher or lower prevalence of autism in the U.S. with proximity to waste incinerators, as was indicated in Figure 1 and accompanying text; if effects of developmental toxins in incinerator emissions are found only in children who receive concentrated, accumulated doses of the toxins via lactation, as apparently occurred in this study, that could have important public health implications.)
Section 6.c: Toxins from incinerator emissions: gradual maternal accumulation, concentration, and relatively rapid excretion:
As pointed out in Section 4, incinerator emissions contain not only dioxins but also mercury, PBDEs, and PCBs. All of those are developmental toxins,24 and most of them are fat-soluble and persistent and therefore they accumulate in human fat tissue; all of them enter breast milk.25 Even though levels of dioxins in breast milk in a number of countries have been declining since the 1960’s, dioxins have still been found to be present in breast milk in concentrations scores to hundreds of times higher than the relatively safe reference dose (RfD) established by the U.S. EPA; continuing high levels of dioxins have been found in studies from many countries carried out during the 2000’s.26 Dioxin has also been found to be present in breast milk at over 100 times the concentration in infant formula.27
Slow accumulation over the mother's lifetime, and relatively rapid excretion: As an illustration of the slow accumulation and rapid transfer of dioxin that normally take place: A 2008 study of breast cancer risk factors looked into concentrations of dioxins that were measured in tissues of 27 infants that had died; information was gathered about birth order and breastfeeding history of the deceased infants. It was found that the closer the infant had been to first in birth order, the higher the dioxin concentrations in the deceased infants’ tissues, “thus showing” (according to the study’s authors) “that the mothers can decontaminate themselves by breast feeding.” 28 The later-born infants were breastfed lower concentrations of the mother's lifetime accumulations of dioxins because of previous transfers of the toxins to earlier-born infants.
There can be little doubt that the predominant transfer of these toxins is lactational, not gestational. See "Postnatal versus gestational...." farther down.
Another illustration of the above-described pattern, of a mothers' lifetime accumulations of toxins being significantly drawn down by each course of lactation, is provided by this chart from a 2008 study:
Many other studies, also, have verified this pattern of a mother's long-term accumulations of "persistent" developmental toxins being significantly excreted during the breastfeeding of each successive child.28a (Perhaps not by coincidence, autism diagnoses have been found in multiple studies to be highest among first-born children and lower with later birth order.28a)
Figure 3 above shows concentrations in human milk according to number of children, and the filled-in, longer-term trend of the woman's levels of the toxins, incorporating those separate measurements, is illustrated here:
Illustration of the long-term trend of a mother's concentrations of PCBs:
The red lines are intended to represent PCB levels in the mother during the successive lactation periods as shown farther above in Figure 3.
Relatively rapid excretion of the long-term accumulations, in concentrated form, is demonstrated in the above studies and in others to follow. That is apparently the way the process works, with fat-soluble, persistent toxins such as those discussed here. Studies have observed that nursing infants consume a daily TEQ (toxic equivalency, used in reference to dioxins) intake that is 50 times higher than that of adults.34 One study team estimated PBDE intake from food to be 0.9 ng/kg/day in adult females, compared with 307 ng/kg/day received by nursing infants.35 A German government commission reported that the average daily PCB intake of an adult is 0.02 micrograms per kg of body weight, as compared with the intake of a breastfed infant (3 micrograms per kg of body weight), which is 150 times higher.36 For indication of major lactational transfer of mercury, compared with much smaller prenatal transfer, see text below Figure 6. It should not be surprising that, in the Lung et al. study (in Section 5), children breastfed for at least six months were found to show traits of neurodevelopmental disorders while other children did not, on average.
It is relevant to note that, according to a major document of the American Academy of Pediatrics published in 2012, referring specifically to PCBs, PBDEs, and major types of pesticides, "Infant formula is free of these residues...." (then going on to explain how that result comes about).36a
Section 6.d: Findings from the above studies are very compatible with what appears to happen with breastfed children in areas of waste incinerator pollution, as follows:
-- An infant would be exposed to toxins from incinerator emissions mainly via the rapid lactational transfer of long-term maternal accumulations of pollutants from the incinerators.
As indicated in Figure 3 and in other evidence cited above, considerable amounts of some major toxins are transferred to infants during lactation while comparatively little is taken in by the mothers during their child-bearing years. According to the U.S. Department of Agriculture, over 90% of human intake of dioxins and dioxin-like compounds (which include some types of PCBs) is via food; 33a that leaves only a small percentage to be shared between inhalation and other means of absorption. The U.S. ATSDR indicates over-150-times-greater intake of mercury via food than via air,32 as well as other evidence indicating that absorption of mercury is predominantly via food.33
Intake of PCBs (chemical relatives of dioxins and PBDEs) is also hundreds of times greater via breastfeeding than during prenatal exposures, according to the ATSDR and a publication of the U.S. National Academies Press.33b For mercury, the postnatal versus prenatal exposure ratio is less extreme but still substantial. (see postnatal mercury transfer..." below.)
An overview of what is happening:
a) Inhalation of polluted air would be only a very minor pathway for absorption of these toxins. That applies especially to a developing infant, whose small lungs would be taking in relatively little of the toxins during the period that is especially developmentally vulnerable (the first year after birth -- see Figure 6 below).
b) However, good evidence indicates that those airborne emissions have nevertheless been having substantial effects of increasing autism diagnoses, despite being a slow, minor pathway of direct exposure.
The superficial incompatibility between (a) and (b) above becomes understandable when realizing that
c) major exposures to infants could result from emissions that have been taken in by full-size (mother's) lungs and slowly accumulated over many years (Section 6.c above), before being excreted rapidly in substantial amounts to small, developing infants via lactation. (see Figure 3 and accompanying text and "postnatal versus gestational..." below).
Observe below the highly vulnerable early-postnatal period of rapid brain development, occurring at the time when a large part of a mother's lifetime accumulations of developmental toxins could be either (a) rapidly entering the infant via lactation, or (b) not doing so.
In addition to the above, there is substantial other evidence of special vulnerability of the developing brain during the first year or so after birth,28b as well as considerable other evidence of special sensitivity to toxins during the earliest weeks and months after birth.28c
It should not be difficult to see connections between long-term intake of dioxins by fully-grown bodies, rapid transfer of the accumulated toxins to infants via lactation during a period of high vulnerability of development, and neurological effects in those infants.
Minor absorption of these toxins via inhalation, but major intake via food:
The U.S. ATSDR indicates over-150-times-greater intake of mercury via food than via air;32 that agency also provides other evidence indicating that absorption of mercury is predominantly via food.33 According to the U.S. Department of Agriculture, over 90% of human intake of dioxins and dioxin-like compounds (which include some types of PCBs) is also via food.33a Therefore, when considering harm that may be done to infant development by emissions of dioxins and related chemicals from incinerators, it makes sense to consider any means by which toxins in airborne emissions can become part of food ingested by infants. That is, in fact, what happens before and during the process of lactation: The toxins are taken in gradually over many years, by way of exposure to gases and dusts from incinerator emissions, and those toxins are slowly accumulated during those many years, by women who will eventually become breastfeeding mothers with those toxins incorporated into their milk. 25
So, as indicated by very substantial evidence, infants living in the vicinities of waste incinerators and other emission sources can (depending on their feeding type) receive either
(a) just the original, direct exposure from the environment, or
(b) that original exposure plus a far greater additional exposure via lactational transfers from accumulated burdens in their mothers.
There is a widespread notion to the effect that the only transfers from the mother that really matter are prenatal, but that idea is misguided. A publication of the U.S. National Academy of Sciences states, "The brain develops steadily during prenatal and early postnatal periods, which are considered as the most vulnerable windows for effects of environmental exposures."37 (italics added) A commission of the U.S. National Research Council (of the National Academies), when discussing “specific periods in development when toxicity can permanently alter the function of a system,” states that the developing brain and certain other organs “may demonstrate particular sensitivity during the postnatal period.”38 Statements by the U.S. Agency for Toxic Substances and Disease Registry (ATSDR) and by academic experts also point to postnatal periods of special vulnerability to toxins.39
Although statements are made on both sides of whether sensitivity to toxins is greater prenatally or postnatally, there appears to be no question about when the greater exposures take place. The U.S. ATSDR states that "the amount of PCBs transferred to offspring is expected to be higher during breastfeeding than during gestation;" and they illustrate that point by describing a laboratory test in which, following administration of PCBs to a female rat before pregnancy, the sucklings received 1600 times as much PCB as was received via transfer to fetuses.40 (Bear in mind that PCBs are related to dioxins and PBDEs, and that they all share many of the same properties.) In human studies summarized in a publication of the National Academies Press, the comparisons that were most relevant to the above pattern yielded ratios of about 280 to 1 and 775 to 1;41 the specific comparisons in those cases were of PCB concentrations in breast milk in relation to PCB contents in umbilical cord serum and cord blood; so the actual total ingestions of PCBs by infants would obviously be determined by how long breastfeeding continued; the postnatal/prenatal ratio for total exposure could very possibly be well over 1000 to 1 with extended breastfeeding.
Postnatal mercury transfer to infants versus prenatal: Mercury excretion via breast milk has been found in many studies to rapidly draw down the mother's accumulated burden.29 A 1998 German study found that concentrations of mercury in breast milk of 85 lactating women at just two months after birth had declined by an average of over 70% from their levels at time of birth.30 A study of prenatal transfers found that mercury levels of over a hundred women were the same at gestational week 37 as at gestational week 12.42 (Mercury in infant formula has been found to normally be less than one-tenth as high as in human milk.31)
Remember from Section 4 the adverse neurological effects of postnatal levels of dioxins, as found in various studies, and the EPA statement about “the most sensitive outcome” of PBDE exposure being “adverse neurobehavioral effects following exposure during the postnatal period."
Section 7: Could something else also be contributing to the large regional differences in autism prevalence?
Although major exposures to mercury and waste incineration emissions were seen (in Figure 1) to be unusually low in the Southeast compared with the rest of the eastern U.S., the exposures in the Southeast are not unusually low compared with those in the western half of the U.S.2 So additional explanation is needed as to why autism in the Southeast should be 50% lower than the U.S. average.
As discussed earlier, there is evidence indicating that toxic exposures that appear to be linked to autism (Sections 3 and 4) only become potent after accumulating in mothers and becoming concentrated (Section 6), before being transferred to infants via breastfeeding. The U.S. CDC provides data about breastfeeding rates, broken down by states, for years going back as far as 2007; 2007 is a relevant birth year in relation to the later autism diagnoses dealt with in the Hoffman et al. study discussed earlier, and that year's data shows that the twelve states of the U.S. Southeast had a mean 12-month breastfeeding rate that was a third below the national average.43
There are also major regional differences in exclusiveness of breastfeeding that would combine with differences in duration of breastfeeding (mentioned just above) to produce greater total transfers of developmental toxins. The limited regional data about exclusiveness of breastfeeding that is available (from the CDC, again43) shows that general exclusiveness of breastfeeding is also well below average in the Southeast. So the total reduction in lactational exposures to developmental toxins in the Southeast is likely to greatly exceed the 33% reduction that was seen in the 12-month breastfeeding rates, compared with average exposure in the U.S. Bearing in mind that breastfeeding-or-not was associated with dramatic differences in autism-related effects of incinerators (Section 6), and noting the evidence about contents of the emissions that could contribute to autism (Section 4), a 50% lower rate of autism in the Southeast might well be explainable by lower total breastfeeding exposure in that region.
Section 8: Other evidence linking early-life exposures in the U.S. to autism according to locations:
There are substantial additional reasons to see links between breastfeeding, according to location, and autism. A 2011 study that investigated data from all 50 U.S. states and 51 U.S. counties found that "exclusive breast-feeding shows a direct epidemiological relationship to autism," and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism." 45 To read much more about other studies with findings pointing in this direction, go to Section 4 of www.pollution-effects.info. To read much more about correlations between geographic locations and autism rates, go to www.pollutionaction.org/breastfeeding-and-autism-and-cancer.htm.
As the author of the above, my role has not been to carry out original research, but instead it has been to read through very large amounts of scientific research that has already been completed on the subjects of environmental toxins and infant development, and then to summarize the relevant findings; my aim has been to put this information into a form that enables readers to make better-informed decisions related to these matters. The original research articles and government reports on this subject (my sources) are extremely numerous, often very lengthy, and are usually written in a form and stored in locations such that the general public is normally unable to learn from them.
My main qualification for writing these publications is ability to find and pull together large amounts of scientific evidence from authoritative sources and to condense the most significant parts into a form that is reasonably understandable to the general public and also sufficiently accurate as to be useful to interested professionals. My educational background included challenging courses in biology and chemistry in which I did very well, but at least as important has been an ability to correctly summarize in plain English large amounts of scientific material. I scored in the top one percent in standardized tests in high school, graduated cum laude from Oberlin College, and stood in the top third of my class at Harvard Business School.
There were important aspects of the business school case-study method that have been helpful in making my work more useful than much or most of what has been written on this subject, as follows: After carefully studying large amounts of printed matter on a subject, one is expected to come up with well-considered recommendations that can be defended against criticisms from all directions. The expected criticisms ingrain the habits of (a) maintaining accuracy in what one says, and (b) not making recommendations unless one can support them with good evidence and logical reasoning. Established policies receive little respect if they can’t be well supported as part of a free give-and-take of conflicting evidence and reasoning. That approach is especially relevant to the position statements on breastfeeding of the American Academy of Pediatrics and the American Academy of Family Physicians, which statements cite only evidence that has been
(a) selected, while in no way acknowledging the considerable contrary evidence,a1 and
(b) of a kind that has been authoritatively determined to be of low quality. (See the paragraphs dealing with observational studies near the end of Section 10 above.)
When a brief summary of material that conflicts with their breastfeeding positions is repeatedly presented to the physicians’ associations, along with a question or two about the basis for their breastfeeding recommendations, those associations never respond. That says a great deal about how well their positions on breastfeeding can stand up to scrutiny.
The credibility of the contents of the above article is based on the authoritative sources that are referred to in the footnotes: The sources are mainly U.S. government health-related agencies and reputable academic researchers (typically highly-published authors) writing in peer-reviewed journals; those sources are essentially always referred to in footnotes that follow anything that is said in the text that is not common knowledge. In most cases a link is provided that allows easy referral to the original source(s) of the information. If there is not a working link, you can normally use your cursor to select a non-working link or the title of the document, then copy it (control - c usually does that), then “paste” it (control - v) into an open slot at the top of your browser, for taking you to the website where the original, authoritative source of the information can be found.
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1) Hoffman et al., Geographic patterns of autism spectrum disorder among children of Nurses' Health Study II women, Am J Epidemiol, Oxford Academic, Published: 19 May 2017 at https://academic.oup.com/aje/article-abstract/doi/10.1093/aje/kwx158/3836018/Geographic-patterns-of-autism-spectrum-disorder?redirectedFrom=fulltext
2) Butler et al., Mercury in the Environment and Patterns of Mercury Deposition from the NADP/MDN Mercury Deposition Network, Jan. 2007, at http://www.arl.noaa.gov/documents/reports/MDN_report.pdf
3) See https://climate.ncsu.edu/edu/k12/.atmosphere_circulation
Also Geier DA et al., Blood mercury levels in autism spectrum disorder: Is there a threshold level? Acta Neurobiol Exp (Wars). 2010;70(2):177-86, http://www.ncbi.nlm.nih.gov/pubmed/20628441
5) Center on the Developing Child, Harvard Univ.: The Science of Early Childhood Development, at http://developingchild.harvard.edu/wp-content/uploads/2015/05/Science_Early_Childhood_Development.pdf
6) Gilbert et al., Neurobehavioral effects of developmental methylmercury exposure, Environ Health Perspect. 1995 Sep;103 Suppl 6:135-42, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1518933/ On p. 136: "In humans, MeHg brain levels are approximately six times higher than blood mercury levels (22)."
-- Also see Magos, The absorption, distribution and excretion of methylmercury. In: The Toxicity of Methylmercury (Eccles CV, Annau Z, Eds) Baltimore: Johns Hopkins University Press, 1987; 24-44.
-- Also U.S. Agency for Toxic Substances and Disease Registry web page at http://www.atsdr.cdc.gov/training/toxmanual/modules/4/lecturenotes.html, saying "Methyl mercury is the most toxicological form of the element and, by its accumulation in the central nervous system (CNS), may result in neurotoxic effects…."
-- Also Burbacher et al., Comparison of Blood and Brain Mercury Levels in Infant Monkeys Exposed to Methylmercury or Vaccines Containing Thimerosal, (Oral Mg Kinetics section) Environ Health Perspect. 2005 August; 113(8): 1015–1021, PMCID: PMC1280342 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1280342
7) Mahaffey et al., Blood Organic Mercury and Dietary Mercury Intake: National Health and Nutrition Examination Survey, 1999 and 2000, Environmental Health Perspectives, volume 112 | number 5 | April 2004, top lines of Tables 2 and 4, 75th, 90th and 95th percentile columns, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241922/pdf/ehp0112-000562.pdf ; the authors point out that organic mercury in human blood is predominantly methylmercury.
-- Also, according to 2003 data from the U.S. National Center for Health Statistics, among the many women who have total blood mercury levels exceeding the safe level established by the EPA (5.8 mcg/L), over 90% of the total mercury was found to be “organic/methyl mercury.” See Figure 1 of Mahaffey et al. study just cited.
-- A Swedish study found that about half of the mercury in breast milk was methylmercury (p. 462 of U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury.
9) Mercury Study Report to Congress c7o032-1-1, Office of Air Quality Planning & Standards and Office of Research and Development Volume VII, Section 184.108.40.206, at http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf
10) Mahaffey et al., Blood organic mercury and dietary mercury intake: National Health and Nutrition Examination Survey, 1999 and 2000, Environ Health Perspect. 2004 Apr;112(5):562-70.at http://www.ncbi.nlm.nih.gov/pubmed/15064162
11) McCann, Mercury Levels in Blood from Newborns in the Lake Superior Basin, GLNPO ID 2007-942 November 30, 2011, at http://www.health.state.mn.us/divs/eh/hazardous/topics/studies/glnpo.pdf According to the author, “the percentage of participants with mercury levels above the RfD in this study (in the U.S. Midwest) is similar to that for women of childbearing age who participated in (U.S.) National Health and Nutrition Examination Survey (NHANES) (Mahaffey et al., 2009).”
13) Environmental Endocrine Disruption: An Effects Assessment and Analysis, by Thomas Crisp and 12 other researchers with the EPA, in Environmental Health Perspectives, Vol. 106, Feb. 1998, Supplement. P. 27 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1533291/pdf/envhper00536-0026.pdf
39) Meeker et al., Exposure to polychlorinated biphenyls (PCBs) and male reproduction, Syst Biol Reprod Med. <#> 2010 Apr;56(2):122-31. doi:10.3109/19396360903443658, at http://www.ncbi.nlm.nih.gov/pubmed/20377311
43) Kaya et al., Mixture of Polychlorinated Biphenyls on Sex-Dependent Behaviors and Steroid Hormone Concentrations in Rats: Dose–Response Relationship, Toxicology and Applied Pharmacology , Jan. 2002, at http://www.ncbi.nlm.nih.gov/pubmed/11814327
17) Lee et al., Association of serum concentrations of persistent organic pollutants with the prevalence of learning disability and attention deficit disorder, J Epidemiol Community Health 2007;61:591–596. doi: 10.1136/jech.2006.054700, Tables 2 and 3, at http://jech.bmj.com/content/61/7/591.full.pdf+html. See the “Adjusted OR” line, with “Referent” (meaning 1) for the groups with non-detectable dioxins, versus the Adjusted OR’s for the groups with detectable dioxins. (In each chart, the second and third chemicals listed are dioxins).>>
18) <<P. 6 of Wyrzykowska-Ceradini et al., Waste combustion as a source of ambient air polybrominated diphenylethers (PBDEs), Atmospheric Environment xxx (2011) 1e7, >>
19) ATSDR: Public Health Statement for PBDEs, CAS#: 67774-32-7, (summary chapter from the Toxicological Profile for PBDEs) at http://www.atsdr.cdc.gov/phs/phs.asp?id=1449&tid=183
20) 2009 EPA Polybrominated Diphenyl Ethers Action Plan at http://www.epa.gov/sites/production/files/2015-09/documents/pbdes_ap_2009_1230_final.pdf, p. 12
Re: breastfed infants’ exposures to dioxins, in many nations:
- Lorber et al., Infant Exposure to Dioxin-like Compounds in Breast Milk, Vol. 110 No. 6, June 2002, Environmental Health Perspectives at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download, indicating 242 pg of TEQ/kg-d at initiation of breastfeeding.
- J Grigg, Environmental toxins; their impact on children’s health, Arch Dis Child 2004; 89:244-250 doi:10.1136/adc.2002.022202 at http://adc.bmj.com/content/89/3/244.full
-- U.K. Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment: COT Statement on a toxicological evaluation of chemical analyses carried out as part of a pilot study for a breast milk archive, 2004, Table 1 and item 41, at http://cot.food.gov.uk/pdfs/cotsuremilk.pdf
- Costopoulou, Infant dietary exposure to dioxins and dioxin-like compounds in Greece, Food and Chemical Toxicology Volume 59, September 2013, Pages 316–324, at http://www.sciencedirect.com/science/article/pii/S0278691513003803
- Focant et al., Levels of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and polychlorinated biphenyls in human milk from different regions of France, Science of The Total Environment, Volumes 452–453, 1 May 2013, Pages 155–162 abstract at http://www.sciencedirect.com/science/article/pii/S0048969713002404
- Yang J, et al., PCDDs, PCDFs, and PCBs concentrations in breast milk from two areas in Korea: body burden of mothers and implications for feeding infants. Chemosphere. 2002 Jan;46(3):419-28. At www.ncbi.nlm.nih.gov/pubmed/11829398
- Bencko V et al., Exposure of breast-fed children in the Czech Republic to PCDDs, PCDFs, and dioxin-like PCBs. Environ Toxicol Pharmacol. 2004 Nov;18(2):83-90. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/21782737/
- Nakatani T, et al., Polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and coplanar polychlorinated biphenyls in human milk in Osaka City, Japan Arch Environ Contam Toxicol. 2005 Jul;49(1):131-40. Epub 2005 Jun 22. Found at http://www.ncbi.nlm.nih.gov/pubmed/15983863
- Chovancová J, et al., PCDD, PCDF, PCB and PBDE concentrations in breast milk of mothers residing in selected areas of Slovakia Chemosphere. 2011 May;83(10):1383-90. doi: 10.1016/j. At www.ncbi.nlm.nih.gov/pubmed/21474162
- Deng B, et al., Levels and profiles of PCDD/Fs, PCBs in mothers' milk in Shenzhen of China: estimation of breast-fed infants' intakes.Environ Int. 2012 Jul;42:47-52.. At www.ncbi.nlm.nih.gov/pubmed/21531025
27) Infant Exposure to Dioxin-like Compounds in Breast Milk Lorber and Phillips Vol. 110., No. 6 June 2002 • Environmental Health Perspectives at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240886/pdf/ehp0110-a00325.pdf, 242 pg at initiation; this should be compared with data from following: U.K. Food Standards Agency Food Survey Information Sheet 49/04 Mar. 2004, Dioxins and Dioxin-Like PCBs in Infant Formulae, found at www.food.gov.uk/multimedia/pdfs/fsis4904dioxinsinfantformula.pdf
Compatible figures were found in Weijs PJ, et al., Dioxin and dioxin-like PCB exposure of non-breastfed Dutch infants, Chemosphere 2006 Aug;64(9):1521-5. Epub 2006 Jan 25 at www.ncbi.nlm.nih.gov/pubmed/16442144
29) Exploration of Perinatal Pharmacokinetic Issues Contract No. 68-C-99-238, Task Order No. 13 Prepared for EPA by: Versar, Inc. EPA/630/R-01/004, Section 220.127.116.11, at www.epa.gov/raf/publications/pdfs/PPKFINAL.PDF According to these researchers contracted by the EPA, "a wealth of information" indicates that lactational transfer of maternal mercury during the first 15 days of lactation is equal to about a third of the total transfer of mercury that takes place during gestation.
-- Wigle, D.T., MD, PhD, MPH: Child Health and the Environment, Oxford University Press, 2003, Ch. 5. p. 106 (typically available through Ebsco Host at local libraries) Stated that the half-life of methylmercury in the blood of lactating women is about half that in nonlactating women, apparently due to excretion in breast milk.
-- Mercury Study Report to Congress c7o032-1-1, EPA Office of Air Quality Planning & Standards and Office of Research and Development Volume VII, Section 18.104.22.168, at http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf According to this EPA article, “Lactating women have shorter biological half-lives for methylmercury (average value 42 days), compared with nonlactating women (average value 79 days) (Greenwood et al., 1978). This is presumably a reflection of excretion of mercury into milk.”
-- Vahter et al., Longitudinal Study of Methylmercury and Inorganic Mercury in Blood and Urine of Pregnant and Lactating Women, as Well as in Umbilical Cord Blood, Environmental Research, Section A 84, 186}194 (2000) at http://www.detoxmetals.com/content/FISH/FISH/Hg%20in%20pregnant%20urine%20and%20cord.pdf According to this 1999 Swedish study, “there was a marked decrease in I-Hg (inorganic mercury) in (the mothers’) blood and urine during lactation, most likely related to the excretion of I-Hg in milk…. About 10% of the Hg (mercury) present in circulating blood (5 L]0.3 lg/L) would be transferred to the milk every day.” (Obviously, the mother also keeps taking in mercury.)
-- U.S. Hazardous Substances Data Bank of the National Library of Medicine's TOXNET system, at http://toxnet.nlm.nih.gov. Evidence from the Iraqi poisoning incident showed that lactation decreased blood mercury clearance half-times in women by 44%, indicating rapid excretion of mercury in breast milk.
-- P. Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants, Environmental Health Perspectives, accepted Oct. 1993 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1567218/pdf. In this study by a prominent scientist (P. Grandjean) and his team, it was found that total mercury concentrations in infants that had been breastfed for one year were three times as high as those in infants that had not been breastfed.
-- Marques RC, et al., Hair mercury in breast-fed infants exposed to thimerosal-preserved vaccines. Eur J Pediatr. 2007 Sep;166(9):935-41. Epub 2007 Jan 20 This study found that mercury measured in infants’ hair increased 446% during the first six months of breastfeeding, while mercury measured in the mothers’ hair decreased 57%. These measurements included mercury from vaccines (still containing mercury at that time in Brazil, where the study was carried out), which the authors estimated accounted for about 40% of the infants’ exposure during those six months. Given that, combined with the finding in a Taiwanese study that over 95% of an infant’s exposure to mercury was from breastfeeding (Chien et al., 2006), the increase in the infants’ mercury levels attributable to breastfeeding was probably well over 200% during the first 6 months of breastfeeding.
-- Rice et al., Environmental Mercury and Its Toxic Effects, J Prev Med Public Health. 2014 Mar; 47(2): 74–83, doi: PMCID: PMC3988285 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988285 According to these experts, the average whole body biological half-life of inhaled mercury is approximately 60 days, but it is estimated that the half-life of mercury in the brain can be as long as 20 years. The above findings of doubling and tripling of mercury levels in breastfed infants would have been based on levels in the whole body, where half-lives are relatively short and accumulation relatively minor, as opposed to levels in the especially vulnerable developing brain, where accumulation would be far greater.
31) Mercury levels in breast milk:
- U.S. ATSDR document on mercury at www.atsdr.cdc.gov/toxprofiles/tp46-c5.pdf, p. 443
Mercury in infant formula:
- Food Additives & Contaminants: Part B: Surveillance Volume 5, Issue 1, 2012 Robert W. Dabeka et al., Survey of total mercury in infant formulae and oral electrolytes sold in Canada DOI: 10.1080/19393210.2012.658087 at http://academic.research.microsoft.com/Publication/57536306/survey-of-total-mercury-in-infant-formulae-and-oral-electrolytes-sold-in-canada
32) Table 5-12, p. 432 of U.S. ATSDR: Toxicological Profile for Mercury, 1999, Ch. 5, Potential for Human Exposure, at http://www.atsdr.cdc.gov/toxprofiles/tp46.pdf This table shows total daily intake of mercury in adults to be 0.04 micrograms per day via air exposure, compared with 6.6 micrograms per day via food.
33) The ATSDR also observed that "dermal uptake of mercury adsorbed to soil is likely to be minor compared to other exposure pathways;" referring to mercury intake via food, the ATSDR adds that "the more lipid soluble organic mercury compounds (e.g., methylmercury) are almost completely absorbed." (pp. 465 and 466 of U.S. ATSDR: Toxicological Profile for Mercury)
33a) Centers for Epidemiology and Animal Health, Animal and Plant Health Inspection Service, USDA: Dioxins in the Food Chain, at http://www.aphis.usda.gov/animal_health/emergingissues/downloads/dioxins.pdf
33b) The U.S. ATSDR, when stating that transfers of developmental toxins are expected to be higher during breastfeeding than during gestation, illustrates that by describing a laboratory test in which the sucklings received 1600 times as much PCB as was received via transfer to fetuses, from the same original pre-gestation dose. (U.S. ATSDR, Persistent chemicals found in breast milk, Appendix A, p. 180, at https://www.atsdr.cdc.gov/interactionprofiles/ip-breastmilk/ip03-a.pdf)
In human studies summarized in a publication of the National Academies Press, the comparisons that were most relevant to the above pattern yielded ratios of about 280 to 1 and 775 to 1; (18) National Academies Press, Hormonally Active Agents in the Environment (1999), Chapter: 6: Neurologic Effects, at http://www.nap.edu/read/6029/chapter/8#178, p. 178. Describing studies measuring maternal concentrations of developmental toxins in 313 women in Michigan, this publication states, “The mean concentrations of PCBs were 6 ng/mL in maternal serum, 3 ng/mL in cord serum, and 841 ng/g in breast milk.”(p. 178) From a German study (Winneke et al., 1998), “Mean concentrations of PCBs were 0.55 ng/mL in cord blood and 427 ng/g in the fat of breast milk.” (p. 183) (1 mL is about the same as 1 g when discussing a substance whose weight is about the same as that of water.)
The specific comparisons in those cases were of PCB concentrations in breast milk in relation to PCB contents in umbilical cord serum and cord blood; so the actual total ingestions of PCBs by infants would obviously be determined by how long breastfeeding continued; the postnatal/prenatal ratio for total exposure could very possibly be over 1000 to 1 with extended breastfeeding.
36) Kommission “Human-Biomonitoring” des Umweltbundesamtes: Stoffmonographie PCB - Referenzwerte für Blut, Section 8.3., found within https://www.umweltbundesamt.de/sites/default/files/medien/377/dokumente/pcbblut.pdf, website of Umwelt Bundes Amt (German Federal Environmental Office). The text drawn on says, " "Die derzeit durchschnittlich vom Erwachsenen täglich aufgenommene Menge an PCB (ca. 0,02 μg PCB/kg KG ) liegt deutlich unter der ATD von 1 μg PCB/kg KG. Der gestillte Säugling erhält dagegen eine deutlich höhere PCB-Zufuhr (3 μg PCB/kg KG.", which Bing Translator very respectably translates as " "The amount taken daily average currently by the adults of PCB (approx. 0.02 μg PCB/kg bw ) is well below the ATD of 1 μg PCB/kg. The breastfed infant, however, receives a significantly higher PCB intake (3 μg PCB/kg bw.)"
36a) American Academy of Pediatrics: Pediatric Environmental Health, 3rd Edition, 2012, p. 200.
37) Dadvand et al., Green spaces and cognitive development in primary schoolchildren, Proceedings of the National Academies of Sciences of the United States of America, Vol. 112,
38) Commission on Life Sciences, National Research Council: Pesticides in the Diets of Infants and Children, p. 43, National Academy Press, Washington, D.C. 1993, at http://www.nap.edu/openbook.php?record_id=2126&page=43
40) U.S. ATSDR, Persistent chemicals found in breast milk, Appendix A, p. 180, at https://www.atsdr.cdc.gov/interactionprofiles/ip-breastmilk/ip03-a.pdf
41) National Academies Press, Hormonally Active Agents in the Environment (1999), Chapter: 6: Neurologic Effects, at http://www.nap.edu/read/6029/chapter/8#178, p. 178. Describing studies measuring maternal concentrations of developmental toxins in 313 women in Michigan, this publication states, “The mean concentrations of PCBs were 6 ng/mL in maternal serum, 3 ng/mL in cord serum, and 841 ng/g in breast milk.”(p. 178) From a German study (Winneke et al., 1998), “Mean concentrations of PCBs were 0.55 ng/mL in cord blood and 427 ng/g in the fat of breast milk.” (p. 183) (1 mL is about the same as 1 g when discussing a substance whose weight is about the same as that of water.)
42) Vahter et al., Longitudinal Study of Methylmercury and Inorganic Mercury in Blood and Urine of Pregnant and Lactating Women, as Well as in Umbilical Cord Blood, Environmental Research, Volume 84, Issue 2, October 2000, Pages 186–194, Table 1
43) CDC: Breastfeeding Report Card (for 2007) at https://www.cdc.gov/breastfeeding/pdf/2007breastfeedingreportcard.pdf
Regional data about exclusiveness of breastfeeding for over 6 months (indicating highest total exposure) or for less than 3 months (most relevant to the initial period of greatest vulnerability -- see Appendix F of www.pollution-effects.info) is not available from the CDC and (apparently) also not available elsewhere.