Pollution from Waste Incinerators in the U.S. in Relation to Regional Variations in Autism Prevalence
Section 1, intro: Outstandingly high prevalences of autism in different parts of the U.S. are associated with presence or scarcity of waste incinerators:
As found in studies and in data from the U.S. government, autism prevalence in different parts of the U.S. is especially high in areas with concentrations of emissions from waste incinerators. Those emissions and autism both appear to be highest in five distinct, separate areas: Minnesota, Indiana, New England, southern South Carolina, and northern Utah.
Complete text and sources in Section 1.
Section 2, intro: Other evidence linking autism with mercury and other pollutants in incinerator emissions:
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 in Section 2.
Section 3, intro: Other pollutants in incinerator emissions that could contribute to 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. by far, and medical waste incineration is in second place. 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 in reference to dioxins and PCBs. 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, 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 moderately 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 wirh 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 far greater signs of increased risk of traits of ASD, ADHD and other developmental delays. Dioxin exposures via breastfeeding were implicated, according to the authors. Other studies have resulted in similar conclusions. Other neurodevelopmental toxins in incinerator emissions (PBDEs, PCBs and mercury) are similarly implicated. 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:
The twelve states of the U.S. Southeast, where autism is 50% below the U.S. average, have characteristics related to the above. 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. are associated with presence or absence of waste incinerators:
Areas of unusually high prevalence of autism in the U.S.:
-- According to data from the U.S. Department of Education, Minnesota has the highest rate of autism in the entire U.S., by a wide margin.a
-- A U.S. study in the process of being 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."
Fig. 1, repeated
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 eastern half of the U.S..2
Note the yellow ellipses indicating Minnesota, Indiana, and the more populated parts of New England. Observe the very disproportionately large presence of blue symbols inside each of these areas, indicating waste incineration. To be precise, a few of the blue symbols in the areas marked for Minnesota and New England are just outside the borders of the named areas; but considering the frequent directions of the winds in those regions,3 large proportions of the emissions from incinerators in those adjacent areas would travel into Minnesota and New England.
Note that the Minneapolis-St. Paul twin-cities region, containing over half of Minnesota's population, is close to the waste incineration sources in Wisconsin and is also in the middle of considerable in-state sources of such emissions.
A close look at South Carolina in Figure 1 will show a cluster of incinerator emissions sources in the southern part of that state. U.S. Department of Education data for South Carolina shows the State of South Carolina to have autism prevalence that is below the national average.a However, as found in a study by eight researchers from the Medical University of South Carolina, there is reason to see autism in the area of the incinerator cluster area to be far above the U.S. average.a1
The authors said that they found autism prevalence that was "substantially higher than has been previously reported" by those who used the established detection methods; they apparently believed that the reason for the dramatic difference was that their ascertainment methods were superior to those of the educational system and medical reports, rather than being a matter of environmental factors specific to their study area. There are reasons to question the accuracy of ASD prevalence (3.62%) that this study group reported.a2 However, even if the true prevalence were only half as high as this group reported, that would still be over twice as high -- for this section of South Carolina -- as the prevalence reported for the state of South Carolina by the U.S. Department of Education in its 2015-2016 data.a
There is only one noteworthy example of a cluster of incinerator emission sources in the western U.S., but that case is well worth a look; see the northwest section of Utah in Figure 1.b. As in the case of South Carolina, the state's autism prevalence is below the national average; a and again in this case, the specific area of the incineration cluster appears to have autism prevalence far above the national average.
(As above, the contents of Figure 1.b were carefully taken from a web page of the U.S. National Oceanic and Atmospheric Administration.2)
As part of a long-term project of the U.S. CDC (the Autism and Developmental Disabilities Monitoring Project), research was carried out in the section of Utah that is the same as the area heavily affected by waste incinerator emissions.2a (See Figures 1.c and 1.b.) Compared with the average autism prevalence (1.42%) of the other ten U.S. locations where the CDC carried out measurements for its 2014 report,2b prevalence in this section of Utah was found to be 1.86%. The U.S. Department of Education reported a prevalence of 0.67% for Utah as a whole in its 2015-2016 data, which is well below the national average.a
So the reader's attention might reasonably be drawn to the associations between incinerator pollution sources and autism prevalence in several distinct, separate parts of the U.S., as indicated above.
Section 2: Mercury
Section 2.a: Mercury from waste incineration:
Waste incineration appears to be a substantial source of mercury emissions to air. Since waste incinerators are often used to generate electricity, it is relevant to note that, according to 2008-2009 data from New York State, municipal waste combustors emitted 14 times as much mercury per megawatt produced compared with coal-fired power stations.2c And this was after considerable reductions in mercury emissions from such incinerators had already been achieved in recent years.
Section 2.b: Evidence linking mercury 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 expert 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 mercury 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 many infants and children downwind from the waste incinerators whose locations are shown in Figure 1 above.
Section 3: Other pollutants in incinerator emissions that could also contribute to autism prevalence:
In addition to mercury, waste incineration is also known to emit substantial dioxins, PCBs and PBDEs, all of which have been linked to harm to neurological development. According to the most recent estimates of the EPA (for the year 2000), medical waste incineration and municipal waste incineration combined contribute about 42% of all emissions of dioxins to the air.
According to a 2006 Korean study, "remarkably high concentration of PCBs in the flue gas of municipal solid waste incinerators and industrial waste incinerators, after conventional air pollution control measures, was
reported in both Japan and Korea," citing three studies.11g According to a 2015 publication of the State of Washington Department of Health, 600,000 metric tons of PCBs were produced between 1929 and 1979 and used in many products ranging from electrical equipment to caulk to paints to carbonless copy paper; the waste stream (often going to incinerators) still contains considerable PCBs as those products and products containing them wear out and as recycled paper products continue to contain PCBs. Also (continuing from the Washington Department of Health), "PCBs are still unintentionally generated by combustion," and "PCBs may (still) be found as contaminants in a wide range of consumer products because of the presence in several pigments and dyes." In addition, "Given the widespread use of chlorinated compounds such as polyvinylchloride for packaging, tubing, and other applications, incomplete combustion forms a wide range of halogenated compounds such as chlorinated dioxins and furans and PCBs. Most municipal incinerators are not effective in destroying PCBs ...." 11a The EPA in 1984, years after general production of PCBs had stopped in the U.S., estimated that 100,000 pounds of PCBs would continue to be produced unintentionally, 11,000 pounds of which would enter products such as printing ink (therefore printed matter), plastics, paints, and dyes -- therefore in many soon-to-be-incinerated products.11d The Washington Department of Health continued, "in general, PCBs can be produced when chlorine and carbon are present with elevated temperatures...." (which is to say, in agreement with an EPA publication, 11h during most waste incineration) According to the authors of a Korean study, various studies have found PCBs to be generated during the combustion process in municipal waste incineration.11c
Reports from earlier years have likely reflected a false impression of low levels of PCBs in incinerator emissions. According to the 2006 EPA document on sources of releases of dioxin-like compounds, "The development of more sensitive analytical methodologies has enabled researchers in recent years to detect dioxin-like PCB congeners in the stack gases and fly ash from full-scale and pilot-scale MWCs" (municipal waste combustors/incinerators11i) (citing studies from 1993, 1994 and 2001)11h Since these methods of detecting PCBs in stack gases from waste incinerators were first being made known in the mid-1990's, it is reasonable that it would be another several years before the new methods would be sufficiently accepted and disseminated to allow their use in the EPA's required reporting; see below the suddenly large stack emissions of PCBs reported for the year 2000. (Although "point" air emissions are also mentioned below, it was new methods of analyzing emissions from waste incinerators that apparently made the difference between reports of 0 and a report of 2,497 kg of PCBs in U.S. air emissions.)
Notice the "Stack or point air emissions" entry (2,497 kilograms, or 2.75 U.S. tons) for the year 2000. Then note below the significant effects that 5.6-microgram doses of PCB have been found to have on developing monkeys. (5.6 micrograms = one fifth of one millionth of an ounce.)
Doses of about 5.6 micrograms per day of a PCB-containing product were administered to infant monkeys for the first 20 weeks after birth, in a study published in 1999; these exposures were with a mixture "representative of PCBs contained in human breast milk" and at a level considered to be safe by the Canadian Health Protection Branch.11e The whole-blood PCB levels of exposed monkeys at the end of the 20-week exposure were "toward the low end of results from the general human population," according to the authors.
In a later test, "treated monkeys had difficulty learning the task, as measured by the number of sessions required to meet a specified performance criterion." (See Fig. 2.a here) Also, "after making one incorrect response, they persisted in making one or more additional incorrect responses on the same button before switching to the opposite correct one." Similar results were found in other tests administered to the monkeys, including "marked differences between control (comparison) and PCB-treated groups" in test performance, including 2-3 times more inappropriate (inefficient) responses by the PCB-treated group, in a test. Summarizing the results from the various tests administered in this study, the authors stated that "these results taken together reveal learning deficits... and inability to inhibit inappropriate responding in monkeys exposed to PCBs for a short time postnatally with environmentally relevant body burdens. These effects are presumably permanent, because behavioral deficits were observed 2.5 to 5.0 years after cessation of PCB exposure."
The authors' statement (as quoted just above) that the exposures of the test monkeys to PCBs were "environmentally relevant" may deserve a second look, now that 18 years have passed since publication of the study. The doses administered in that study produced infant PCB levels that were similar to or lower than those of "the general human population," which was appropriate at that time, considering typical duration of breastfeeding at that time. As seen in this chart published by the Danish Health and Medicines Authority, the PCB level of a breastfed infant with about 5 months of breastfeeding (a typical duration in the late 1990's) would be about the same as that of the mother. (see ratio of 1 at 22 weeks, in this chart)
But with the great increases that have taken place since then in breastfeeding for six months or more,11k average infant PCB levels could very possibly have come to significantly exceed those of the general population in more recent years (see this chart and reference 11m). And certainly many thousands of individual infants' PCB levels would be far above those of the general population. Therefore the adverse effects of postnatal PCB exposures on developing children could often be significantly greater currently than as were found in the Rice study, described above.
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.” 11f Another research team, who are authors or co-authors of over 540 studies and published articles, wrote a relevant review article with the title, "Polychlorinated biphenyls and the developing nervous system: Cross-species comparisons;" the authors stated that "effects are roughly similar across species, but ... the lowest level based on the neurotoxicology level (was) coming from the human data."11j In other words, human infants are likely to be more sensitive to effects of PCBs than were the monkey infants whose later test results were shown in Figure 2.a above.
The 2,497 kilograms (2.75 tons) of PCBs reported as being released to the air in the U.S. in a single year, mainly from incineration (Figure 2 and accompanying text, above), are sufficient to make over 456 billion doses of the approximate size administered in Rice study discussed above; such doses, ingested daily over a 20-week postnatal period, led to observable adverse effects in the neurological development of monkeys. Clearly, the effects of those tons of airborne PCBs would be expected to be greatest among people (including infants) living in the regions where the most incineration takes place; that is fully compatible with what appears to have actually turned out to be the case, as shown in Section 1.
Medical waste incineration, also, is very much an ongoing source of PCBs to the air, and a source that is more widely distributed in the population than municipal waste incinerators. A 2009 Chinese study found that significant formation of PCBs was taking place in medical waste incineration, and dioxin-like PCBs constituted about 19% of the total PCB concentrations emitted.11b
PBDEs have also 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 This is likely to continue for decades, since PBDEs have been so widely used as flame retardants in home furnishings and other consumer products that will long continue to fed into to incinerators.
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 (See Figure 6 and accompanying text about the highly vulnerable early-postnatal period of brain development.)
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 in relation to increased postnatal background dioxin exposure: "an increase in social problems (p<0.001), thought problems (p=0.005), and aggressive behaviour (p=0.001)," as reported by teachers.15 Bear in mind that problems in social interaction are a core characteristic of ASD, and the other two problem areas mentioned in this study 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 (apparent effects of background dioxin exposures, as found in this study) are common among people with ASD.
As indicated above, average levels of dioxins and PCBs in human milk in most countries are far above established safe levels; exposures resulting from living in areas with waste incinerator emissions would be in addition to these already-high background levels.
Chart above from study at https://link.springer.com/article/10.1007/s00204-016-1802-z
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 mercury, dioxins, PCBs and PBDEs, and increased prevalence of ASD. As indicated in Figures 1 through 1.c and accompanying text, regionally-high levels of autism in the U.S. appear to align very well with high levels of emissions from waste incinerators, with their developmentally toxic contents as discussed above. This should be considered as a possible explanation for existence of various geographic areas of elevated prevalence of ASD, as found in the recent Hoffman et al. study as well as in other data presented in Section 1.
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 appear to be authors or co-authors of over 1600 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 on neurodevelopmental outcomes associated with residence near an incinerator were reported among children in the population residing within three kilometers from the incinerators. The authors measured both by assessing the children’s developmental milestones and by evaluating parental concerns, and "both instruments showed that living near an incinerator increased the risk of U/DDD during child development." (U/DDD was said to include developmental delay, ASD, and ADHD)
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 maps of the 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 made comparisons of development of children according to different possible risk factors. Among children in the general population living within three kilometers of the incinerators, effects were observed (Section 3.2 of study), which 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." (The authors referred to that increased risk among breastfed infants as "indirect effects" of the emissions.) As a proposed explanation for this finding, the authors noted 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.
Section 6.b: Comparison of the effects of lactational exposure to incinerator emissions with direct effects of the emissions:
After the indirect effects of transfers via breastfeeding were separated out in the analysis, "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." (p. 2250) And in the assessments at 36 months, the only direct effect that was found was fairly minor; analysis showed that living near an incinerator was adversely associated only with gross motor development (among four standards measured) at that time.
On the other hand, the authors reported that "through the mediating factor of breastfeeding, the presence of an incinerator was indirectly associated with six-month gross motor... and fine motor ... development and 18-month gross motor..., fine motor..., language ... and social ... development." (in Supplemental Materials) The text omitted in that last sentence (indicated by all the dots) consisted entirely of numbers indicating detailed measurements of the effects and the numerical level of statistical significance of each finding. To help keep this present description from being overly technical, all of those numbers will be summarized here as follows:
a) the strength of the effect found among breastfed children was, in every case, two to five times the strength of the one effect found in children in the general population; and
b) the statistical significance of the findings relating incinerator emissions with developmental problems in breastfed children was very high in every case -- far greater than that of the one effect found in the general population.
And it bears emphasizing that these far greater effects, each with much greater statistical significance, were found in several times as many areas measured, compared with the one effect found in the general population. And those areas of measurement, especially language and social development, were related to common deficits in those with autism.
So there appears to be good evidence suggesting that exposures to pollutants from waste incinerators may have substantial harmful effects on development if those toxins are ingested by infants indirectly via breastfeeding, but the effects are likely to be relatively minor when the toxins are only inhaled directly.
Although indirect effects may usually be less potent than direct effects from the environment, the opposite is the case with respect to many environmental toxins and lactation. Consider what is known about the slow absorption via inhalation of certain toxins that are taken in by a woman over the long-term -- and accumulation of those toxins over the years; long-term accumulations can be rapidly excreted to infants during the process of lactation. That process will be discussed below.
Section 6.c: Toxins from incinerator emissions: how they most effectively reach the developing infant
As pointed out in Sections 3 and 4, incinerator emissions are likely to 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
Gradual 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 exposures..." 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 just above shows concentrations in human milk according to number of children, and just below is an explanatory depiction of the filled-in, longer-term trend of the woman's levels of the toxins, incorporating those separate measurements:
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, was demonstrated in studies referred to above and in others to be described below. 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. incinerator-effects study described above, 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. (see Section 6.c just 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, as indicated in Figure 3 and in other evidence cited above. 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).
As indicated above, exposures to environmental toxins at normal background levels are likely to lead only to relatively small, gradual increases of levels in adults; but a breastfed infant receives exposures that are rapid and large, relative to its size.
The exposures of an infant to these toxins, which are major during its vulnerable developmental period (see Figure 6 below), originated from the same sources to which the mother was exposed with little effect.
(The study from which the above charts were taken33c was carried out by a team of 20 European and Canadian researchers, analyzing seven European birth cohorts.)
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 rapidly entering the infant via lactation.
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
In summary, what we have described here is
a) long-term intakes, by grown bodies, of dioxins and other developmental toxins from incinerator emissions,
b) accumulation of the toxins in women's bodies,
d) those transfers taking place during a period of high vulnerability of development.
It should not be surprising that this process would have more effect on the development of an infant than just the direct exposures to the incinerator emissions, as was found in the Lung et al. study described in Section 6.a and 6.b.
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 also 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 relevant pollutants. 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 residues from incinerator emissions 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 (Sections 6.a and 6.b), 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.
Consider how the discussion above 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.
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.
The reader is strongly encouraged to check the source(s) regarding anything he or she reads here that seems to be questionable, and to notify me of anything said in the text that does not seem to accurately represent what was said by the original source. Write to email@example.com. I will quickly correct anything found to be inaccurate.
For a more complete statement about the author and Pollution Action, please go to www.pollutionaction.org.
Fredericksburg, VA, USA
a.1) Carpenter LA et al., The Prevalence of Autism Spectrum Disorder in School Aged Children: Population Based Screening and Direct Assessment, IMFAR presentation, May 12, 2017, Marriott Marquis Hotel, San Francisco, accessed at https://imfar.confex.com/imfar/2017/webprogram/Paper25414.html
a.2) Alternative screen finds high autism prevalence in U.S. state, the News & Opinion section of SFARI.org, an initiative of the Simons Foundation, at https://spectrumnews.org/news/alternative-screen-finds-high-autism-prevalence-u-s-state/
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
2a) Accessed at https://www.cdc.gov/ncbddd/autism/states/ADDM-Utah-fact-sheet.pdf
2b) Figures for other 10 locations at https://www.cdc.gov/ncbddd/autism/states/Comm_Report_Autism_2014.pdf
2c) Document from New York State Department of Environmental Conservation, p. 25,
3) See Figure B (second layer from top of globe) at https://climate.ncsu.edu/edu/k12/.atmosphere_circulation regarding winds into New England; for winds blowing into Minnesota's Twin Cities area, with over half of the state's population, receiving incinerator emissions from across the state line in Wisconsin (in addition to considerable emissions from within Minnesota), see below:
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).”
11a) Washington State Department of Health: PCB Chemical Action Plan, 2015, at https://fortress.wa.gov/ecy/publications/documents/1507002.pdf, pp. 11, 44, 59
11b) Chen et al., Polychlorinated biphenyls emission from a medical waste incinerator in China, JHazmat 2009, at https://www.researchgate.net/publication/26803055_Polychlorinated_biphenyls_emission_from_a_medical_waste_incinerator_in_China
11c) Shin et al., Concentration and congener patterns of polychlorinated biphenyls in industrial and municipal waste incinerator flue gas..., 2006, at https://www.researchgate.net/publication/7443263_Concentration_and_congener_patterns_of_polychlorinated_biphenyls_in_industrial_and_municipal_waste_incinerator_flue_gas_Korea
11e) Rice DC, Behavioral Impairment Produced by Low-Level Postnatal PCB Exposure in Monkeys, Environmental Research Section A 80, 1999. A breastfeeding macaque monkey weighs an average of about 0.75 kg over the 4-5 month lactation period (The Macaque Website/ Life History/ Infancy, at https://www.nc3rs.org.uk/macaques/macaques/life-history-and-diet/)
.75 micrograms per day per kg of body weight (as administered in this study) times .75 kg of infant body weight equals about 5.6 microg/day.
Also see: 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.
11g) Shin et al., Concentration and congener patterns of polychlorinated biphenyls in industrial and municipal waste incinerator flue gas..., 2006, at https://www.researchgate.net/publication/7443263_Concentration_and_congener_patterns_of_polychlorinated_biphenyls_in_industrial_and_municipal_waste_incinerator_flue_gas_Korea
11h) 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, Section 10.4.1, p. 10-27. at https://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=159286
11i) The EPA uses the terms "municipal waste combustors" and "incinerators" interchangeably; see https://www.epa.gov/stationary-sources-air-pollution/large-municipal-waste-combustors-lmwc-new-source-performance
11j) Tilson et al., Polychlorinated biphenyls and the developing nervous system: Cross-species comparisons. Literature Review, 1990. Available from: https://www.researchgate.net/publication/21041131_Polychlorinated_biphenyls_and_the_developing_nervous_system_Cross-species_comparisons
11k) The Surgeon General’s Call to Action to Support Breastfeeding 2011, Figure 1, p. 7, at www.surgeongeneral.gov/library/calls/breastfeeding/calltoactiontosupportbreastfeeding.pdf
11m) Verner et al., Measured Prenatal and Estimated Postnatal Levels of Polychlorinated, Biphenyls (PCBs) and ADHD-Related Behaviors in 8-Year-Old Children, Environ Health Perspec, Sept. 2015, at http://ehp.niehs.nih.gov/1408084/
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
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 ORs for the groups with detectable dioxins. (In each chart, the second and third chemicals listed are dioxins).
17d) 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 www.thelancet.com/journals/lancet/article/PIIS0140-6736(01)06654-5/abstract
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
20a) EPA's Mercury Study Report to Congress, Vol. 4, at https://www.epa.gov/sites/production/files/2015-09/documents/volume4.pdf
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.
33c) Iszatt et al., Prenatal and Postnatal Exposure to Persistent Organic Pollutants and Infant Growth: A Pooled Analysis of Seven European Birth Cohorts, Environ Health Perspect v.123(7); 2015 Jul at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4492262/
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.