Neurodevelopmental Effects Associated with Air Pollution:
Is the Developing Brain Harmed More Prenatally or Postnatally?
Summary and index:
General thesis: Reports about apparent adverse effects of “prenatal” exposures to atmospheric toxins have not been mentioning the strong likelihood that the harmful exposure of the developing brain to the relevant toxins actually takes place postnatally; specifically, important environmental toxins are known to accumulate in the mother’s adipose tissues and to later transfer to the developing infant via lactation, in much greater postnatal doses compared with prenatal exposure. In addition to the considerable supporting evidence below, it is also relevant that typical U.S. air pollution has been declining substantially while neurodevelopmental disorders (not just autism) have been increasing among children; by contrast, the principal avenue of transfer of recognized toxins to the developing organism, breastfeeding, has been increasing while the disorders have been increasing.
Section 1: Prenatal exposures of developing brains to atmospheric toxins are minimal, whereas postnatal exposures to those same toxins (accumulated in mothers prenatally) are high for most infants
Section 1.a: The particulate matter associated with autism in some studies is emitted into local air together with recognized developmental toxins that come from the same sources.
Section 1.b: Those toxins, once inhaled and absorbed, are known to accumulate in the mother’s body, crossing the placenta only minimally.
Section 1.c: Postnatal exposures of most developing brains to those accumulated pollutants, via breastfeeding, are known to be far higher than prenatal exposures to the same toxins.
Section 1.d: Recent exposures regularly alter the composition of a mother’s accumulated burden of toxins, such that third-trimester exposures to atmospheric toxins are likely to be principal determinants of what is excreted in early breast milk.
Section 2: The infant brain is rapidly developing and vulnerable to toxins after birth.
Section 2a: The developing brain’s postnatal vulnerability to toxins is especially great during the very early weeks after birth.
Section 2.b: There is no satisfactory basis for the belief that neurological development is significantly vulnerable to toxins only prenatally.
Section 3: Major sources of fine particulate matter (mainly combustion of fossil fuels) that are also major sources of mercury, PCBs and PBDEs:
Section 3.a: Sources of fine particulate matter:
Section 3.b: Major sources of mercury that are also sources of PM-2.5
Section 3.c: Major sources of PCBs and PBDEs that are also sources of PM-2.5
Section 3.d: Diesel and urban sources of PCBs and PBDEs that are also sources of PM-2.5
Section 4: Over five-fold differences in atmospheric PCB deposits according to distances from major roads -- PCBs are clearly an important component of PM-containing air pollution.
-- But, unlike particulate matter, PCBs are recognized to be developmentally toxic. And they accumulate in mothers and are transferred to infants in over-15-times higher concentrations after birth than prenatally. It is similar, although to lesser extents, for mercury and PBDEs.
Section 5: Child neurological disorders and air pollution have been trending in opposite directions; but neurological disorders and breastfeeding rates have both increased greatly.
-- Section 5.a: Air pollution has greatly declined while at the very same time neurological disorders “have emerged as major chronic conditions” among children
-- Section 5.b: Breastfeeding, the principal means of delivering neurodevelopmental toxins to the fetus/infant, has greatly increased while neurological disorders among children have “emerged” as major conditions;
-- It is entirely possible that air pollution’s toxic contents become seriously harmful mainly after they become concentrated by the lactation process before being transferred to the developing infant in high doses;
-- by comparison, placental transfer of inhaled developmental toxins is minimal.
Considerable evidence is provided in verification of all the above.
Section 6: Evidence that postnatal exposures of the developing brain to toxins cause neurodevelopmental disorders
-- Section 6.a Three studies specifically linking autism with breastfeeding
-- Section 6.b PCBs; mercury; dioxins
-- Section 6.c Studies linking autism with atmospheric pollution, mainly with postnatal exposures. Exposures to general traffic pollution measured during the year after birth have been found to have far greater effects than exposures measured prenatally.
-- Section 6.d Where breastfeeding is extended, especially high odds ratios for autism related to postnatal toxic exposures
-- Section 6.e When investigating by more precise time periods, especially high odds ratios for autism related to postnatal toxic exposures:
Section 7: Bringing together findings from the three recent, related studies.
-- Two out of three studies found the greatest associations of autism with postnatal exposures of the infant, and the third study did not conflict with the possibility of a strong but brief postnatal effect.
-- Exposures to general traffic pollution measured during the year after birth were found to have far greater effects than exposures measured prenatally.
When studies find associations of autism with prenatal exposures of the mother to pollution, they are also finding associations of autism with postnatal transfers to the infant of toxins that were accumulated outside the fetus before birth. The main difference is that the postnatal doses are many times greater than the prenatal exposures, and those amplified postnatal exposures are received while the brain is still actively developing and vulnerable to toxins.
The postnatal, greatly-increased ingestion of accumulated toxins should therefore be of the greatest concern. That is especially true since the postnatal ingestions, unlike the prenatal exposures, can be rapidly and greatly reduced. Most cows do not have major exposures to the traffic emissions, other combustion emissions, and urban air that are sources of particulate matter and its accompanying toxins. The rarely-breastfed mid-20th-century generation did not have health problems that have become common since then.
Given the findings of two studies published in early 2015, there is good evidence pointing to a likelihood that autism can result from the mother’s exposures to air pollutants during gestation.(Raz et al.,”1 and Kalkbrenner et al.2) That leads to an important next question, which is, how much of the developing brain’s exposure to those toxins takes place prenatally, and how much of the harmful exposure actually takes place postnatally, when accumulations of those toxins are excreted to the infant via lactation? That is an extremely important question to address, especially since postnatal transfers of the toxins are very much subject to reduction by voluntary means.
Section 1: Prenatal exposures of developing brains to atmospheric toxins are minimal, whereas postnatal exposures to those same toxins (accumulated in mothers prenatally) are high for most infants.
Section 1.a: The particulate matter associated with autism in some studies is emitted into local air together with known developmental toxins that come from the same sources
The authors of the Raz et al. study say that they cannot rule out that “another pollutant that co-varies with PM-2.5. Nor can we determine whether there is a particular component of PM-2.5 that is responsible for the associations we found.” They also point out that “airborne particles are covered with various contaminants.”3 Mercury, PCBs, and PBDEs4, all of which are known or strongly-suspected developmental toxins, are known to be emitted by very much the same sources (widespread fossil-fuel combustion processes) that emit PM-2.5 (see Section 3); and all of those are known to become attached to particles as well as to continue in the air space in gaseous form.
Particulate matter is not recognized by the EPA or the NIH to be a developmental toxin.5,6 The lack of finding of developmental harmfulness of that substance is especially significant considering the fact that particulate matter has been extensively studied with respect to its health effects. (see above references)
However, two of the three specific toxins that typically accompany fine particulate matter (PCBs and mercury) are recognized to be neurodevelopmental toxins, and the EPA says there is “substantial evidence” that the third, PCBEs, is a neurodevelopmental toxin.<6a> Those three toxins are known to accumulate in a mother’s body and to be excreted in breast milk; that transfer by lactation occurs at a time when the infant’s ongoing neurological development is highly vulnerable to disruption by chemicals. (See Section 2.a.) Bear in mind the small fraction of maternal PCBs and PBDEs that the fetus receives prenatally, especially compared with the greatly increased concentrations transferred not much later via breast milk (see Section 1.c and linked text).
Mercury, PCBs and PBDEs (accompanying particulate matter -- see Section 3) are known to build up in the mother’s adipose tissues, later to be excreted to the infant in breast milk. (see Section 1.d and footnote 8) It appears that most particulate matter of the kind that has been implicated in the recent studies is unable to cross the placental barrier. Bear in mind that PM-2.5, which was the focus of the Raz et al. study and within the range investigated in the Kalkbrenner study, is 2.5 micrometers in diameter or less; that is the same as 2500 nanometers (nm) or less. A 2008 study found that certain particles that were as small as 30 nm were unable to cross the placental barrier.7 A 2010 study found that another type of particles as large as 240 nm were able to cross the barrier, but the next higher diameter that was tested (500 nm) was unable to cross the barrier.7a So obviously the protectiveness of the barrier varies according to the specific substance. But in any case, it appears probable that most of the particulate matter such as was the focus of these studies is not able to cross the placental barrier. See the next section for indications that the toxins that accompany the particles (or that are attached to them) are also mostly screened out by the placenta.
Section 1.c: Postnatal exposures of most developing brains to those accumulated pollutants, via breastfeeding, are known to be far higher than prenatal exposures to those same toxins.
In a study published in 2003 by a team of five Swedish scientists, it was found that cord blood plasma concentrations of both PCBs and PBDEs were less than one-fifth as high as the concentrations of those toxins in maternal blood plasma; by contrast, those toxins in breast milk were found to be about three times as high as those same toxins in maternal blood plasma;9 that was the same as over 15 times as high in breast milk as in cord blood plasma. A Dutch study found very similar results indicating low cord blood PCB levels in relation to maternal blood levels.10 The above provide more recent evidence confirming an earlier statement (by experts on chemical contamination, A. A. Jensen and S. A. Slorach), "Significantly more (10 to 20 times) of a mother's body burden of persistent organohalogens is transferred to the infant via the milk than by the transplacental route." 11 (PCBs and PBDEs are organohalogen compounds.) Those greatly increased postnatal exposures to a mother’s accumulated burden of PCBs are apparently well absorbed by the developing infant, according to a finding quoted by WHO.12
According to researchers contracted by the EPA, "a wealth of information" indicates that lactational transfer of maternal mercury during the first 15 days after birth is equal to about a third of the total transfer of mercury that takes place during gestation.13 Many other studies and expert statements, to be found in Appendix A, provide compatible evidence indicating that fetal exposures to at least some (if not all) hazardous toxins to which the mother is exposed are minor, especially compared with later exposures of the infant to those same toxins via lactation.
Section 1.d: Recent exposures regularly alter the composition of a mother’s accumulated burden of toxins, such that third-trimester exposures to atmospheric toxins could be principal determinants of what is excreted in early breast milk.
Food is considered to be the main source of PCBs and mercury for the general population; but for mothers who live in areas with increased air pollution, it is likely that inhalation would be the primary source of the toxins accumulated in their bodies, as found in a U.K. study.14 Those toxins are steadily being excreted from the body, but usually at a slower pace than the rate of their entry; therefore they accumulate, mainly in adipose (fat) tissues. Mercury is reported by the NIH to have a half-life in the body of 30 to 79 days.15 PBDEs have been found to have half lives in the body of 11 to 91 days (varying according to the specific type of PBDE).16 PCBs are reported to have widely varying half-lives in the body depending on the particular form of PCB; in a research document provided on the web pages of the Oak Ridge National Laboratory, of five PCB species reported on, three had half lives of less than 90 days and two had half lives of more than 90 days.17 According to the Danish Health and Medicines Authority, the forms of PCBs that are most abundant in food are the more persistent ones (the ones with longer half lives), and that is “much different from the pattern in air.”16a Therefore the types of PCBs that would be of relevance in relation to effects of air pollution would be mainly the types with half lives of less than 90 days. So, in the cases of all three toxins of concern here, which accumulate in the mother’s body, there is considerable turnover within the accumulations from one three-month period to the next; earlier doses are excreted at a moderate rate while the body receives new, often different, exposures.
Therefore, at the beginning of lactation, the mother has accumulations of toxins ready to be mobilized from her fat tissues, but the specific nature of the accumulated burden of toxins is transitory and closely reflects her exposures during the final months of gestation.
It should be remembered that the concentrations in breast milk of the toxins of concern here are apparently far higher than the concentrations in the mother, and especially far in excess of the concentrations to which the fetus is exposed; as indicated with authoritative sources in Section 1.c, two of the three toxins discussed here have been found to be over 15 times as high in breast milk as they were in cord blood, and the third is authoritatively reported to be ingested by infants in the first two weeks of nursing in amounts equal to a third of the entire transmissions of that toxin during gestation. Those three toxins are also normally present in human milk far in excess of authoritatively-determined safe levels, and in concentrations ranging from over 20 times to over 100 times as high as their concentrations in infant formula. (for details, including citations of authoritative sources, see www.autism-research.net/)
Section 2: The infant brain is rapidly developing and vulnerable to toxins after birth.
Section 2.a: The developing brain’s postnatal vulnerability to toxins is especially great during the very early weeks after birth.
The above-described greatly-increased postnatal exposure of the infant brain to toxins comes at a time when its development is continuing and still vulnerable to toxins, according to the EPA, the NIH, and the U.S. ATSDR;18 the early-postnatal period is also the time of the principal vulnerability of the cerebellum to toxins, since most of that region’s development takes place during the early months after birth. (see this chart and also 19, 20, 21) Bear in mind that many studies have found dysfunction or small size of the cerebellum to be associated with autism.22, 23
In the very early weeks following birth, especially great vulnerability of the infant brain to developmental toxins that are then being rapidly transferred to it:
Note that according to EPA researchers, studies “have clearly demonstrated that when proliferation is actively occurring in a given region of the brain, it is vulnerable” to toxins.24 Given that, see the chart just above, and read the following quote with the findings of a 2014 study by twelve scientists: “The growth rate (of the whole brain, at birth) was approximately 1%/d, slowing to 0.4%/d by the end of the first 3 months.”25 That was one percent per day on average right after birth, slowing down greatly by the third month. Early postnatal brain growth (and therefore vulnerability) was found to be even greater among male children, those most affected by ASD and ADHD.
There is still faster brain growth taking place during the first few weeks after birth in specific brain tissues that could be critical to normal development, as indicated by the following:
1) MRI imaging has found that “myelinated white matter” in the developing brain increases five-fold in a brief six-week period ending three weeks after (full-term) birth.26 To learn about the significance of myelination, read the following about the importance of that process from a study by a pair of researchers with the Division of Child and Adolescent Psychiatry of Columbia University: they refer favorably to the hypothesis that “exposure of the developing brain at this time (a few weeks before or after birth) to environmental toxins … disrupt myelination and thereby predispose to poor cognitive, neurodevelopmental, and neuropsychiatric outcomes.”27
2) According to the U.S. ATSDR, in reference to a specific period when injury to neurons resulting from mercury exposure is likely to take place, “Mitosis (the first step of cell division) and migration of granule cells (a type of neurons) in the cerebellum end within weeks following birth.”28 (Remember that dysfunction of the brain’s cerebellum region has been identified in many studies as being implicated with autism.)29
3) A web page of the NIH states that neonatal hypothyroidism, which it says can cause intellectual disability, can result from thyroid levels that are “only slightly low.”30 (“Neonatal” refers to the first four weeks after birth.) Several other authoritative sources concur with the statement of serious consequences of neonatal hypothyroidism, including statements in an Oxford Journal about “devastating functional consequences” and “mental retardation resulting from neonatal thyroid hormone deficiency.”31 , 103
Note in the chart below the effect of typical variations in background levels of mercury on thyroid levels in adults:
Breastfed infants’ mercury exposures are likely to be much higher than normal adult exposures, such as would apply to the chart above, as indicated by the following: a 1998 German study found that concentrations of mercury in breast milk of 85 lactating women at two months after birth had declined by an average of over 70% from their levels at time of birth.32 This large part of a grown person’s mercury burden is rapidly passing to a small infant at a time when the infant is likely to have a “much higher absorption rate” and “lower excretion” of heavy metals, compared with an adult (as found in experiments with animals).33 It should therefore reasonably be expected that the infant’s concentrations, per pound of body weight, would soon greatly exceed those of typical adults. The resulting thyroid reduction in at least some breastfed infants would therefore be expected to be greater than what is shown above for adults.
PCBs and PBDEs are also present in the same polluted air that contains fine particulate matter (see Section 3), and they have also been found to reduce thyroid levels.34, 35 According to an eight-scientist Dutch research team, testing 105 mother-infant pairs, higher PCB levels in human milk correlated significantly with reduced thyroid hormone levels in readings taken at the second week and third month after birth, but especially in the readings taken in the second week after birth.36 A study published in 2007 by a three-scientist American team, with 2445 participants, concluded that “the data show a dose-dependent decrease in total T4 (thyroid hormone) with exposure to TEQs (which are typically present in PCBs) at levels similar to those found in the general U.S. population.” And further, “most studies of exposure to PCBs have found inverse associations with T4.”37 Note that PCB levels in children who had been breastfed for 6 to 12 months were found to be nine times as high as in formula-fed children even at age 3½, in a 2014 study.38
So there is good evidence that thyroid, necessary for development of the brain, is reduced by PCBs and PBDEs as well as mercury. All three of those toxins are emitted by the same sources that emit fine particulate matter (see Section 3), and all three are received by breastfed infants in concentrations far exceeding their prenatal exposures. With all of the above in mind, remember the NIH statement that hypothyroidism in the first weeks after birth, which it says can cause intellectual disability, can result from thyroid levels that are “only slightly low.”
The NIH doesn’t discuss the consequences of neonatal hypothyroidism with reference to ASD, but the long-term consequences as presented by the NIH include traits that strongly resemble frequent traits of ASD: “failure to adapt (adjust to new situations),” “lack of or slow development of motor skills, language skills, and self-help skills,” “difficulty understanding and following social rules,” “failure to grow intellectually or continued infant-like behavior,” and lack of curiosity, as well as difficulty in school.39
For many more authoritative findings about serious long-term consequences of hypothyroidism during the first weeks after birth, see Appendix B; that also contains additional information about autism-resembling outcomes that are likely even if neonatal hypothyroidism is detected and treated, and it includes details about specific autism-linked brain components that are harmed by low thyroid. Appendix B also provides information about reduced neurological optimality having been found in children exposed to PCBs postnatally but not in those exposed prenatally.
It should be of particular concern that the above-described period of especially high vulnerability of the developing brain occurs at the same time that the infant is receiving especially high exposures to developmental toxins that accumulated in the mother earlier (see Section 1.c).
Something else that makes the early postnatal period especially perilous compared with the prenatal period: during gestation, the mother’s thyroid supply can supplement that of the fetus; this helps insure that thyroid-dependent prenatal brain development does not suffer from lack of that hormone. After birth, that external supply is obviously no longer present, at a time when breastfed infants’ own thyroid supplies are being reduced by major increases in toxins ingested, as explained earlier.
So a question that ought to be considered is the following: If a mother receives elevated exposure to toxins during the third trimester of gestation, is there good reason to assume (as many people do) that harmful doses from that exposure are necessarily affecting the developing brain before birth?
Section 2b: There is no satisfactory basis for the belief that neurological development is significantly vulnerable to toxins only prenatally.
There is the widely-held belief that the developing brain is vulnerable to effects of toxins prenatally but not significantly vulnerable postnatally. However, contradicting that notion, the early postnatal period of the brain’s development has been determined to be a time of continued vulnerability to effects of toxins, according to the NIH, the EPA, the U.S. ATSDR (Agency for Toxic Substances and Disease Registry), and at least five experts to whose writings Raz et al. respectfully refer (Grandjean, Landrigan, Rodier, Rice and Barone).40 Kalkbrenner et al. refer to the latter two twice, as well as to Rodier. In addition, at least 17 scientific studies have found that various toxins are associated with greater harm to the developing infant postnatally than prenatally.41 Several of those studies found associations of postnatal exposures specifically with autism and with deficits in autism-related development. Some of the postnatal vulnerability is related to continuation of stages of the brain’s development that are well along before birth and which continue after birth; but other aspects of it are related to phases of the brain’s development that are recognized to take place very predominantly after birth, especially development of the cerebellum. (See Sections 1.b and 2.a above.)
Part of the misunderstanding about postnatal vulnerability of the developing brain arises from that organ’s especially great vulnerability during the very early postnatal period, when its effects may have been confused with effects of prenatal exposures, in earlier research. Researchers often measure toxin levels in umbilical cord blood and/or breast milk and/or in the atmosphere at approximate time of birth and see those as indications of prenatal exposures, not mentioning that those are also indications of far greater exposures to those same toxins that take place right after birth via breastfeeding. (see Section 1.c). Or they see signs of something having gone wrong during a specific brain development process that is known to “mostly” take place before birth (such as migration of brain cells); no mention is made of the fact that those same processes are also known to substantially continue after birth, especially in the autism-implicated cerebellum,42 and at a time when exposures to developmental toxins are far higher than before birth.
Most readers uncritically accept such reports of “prenatal” exposures, or are unaware of the continued postnatal vulnerability of the developing brain or of the huge increases in the developing brain’s exposure to toxins that take place via lactation. So the prevailing belief leads to improper interpretations which in turn lead to self-perpetuation of the prevailing belief.
When researchers do investigate body concentrations of toxins in children during a period that they call “postnatal,” that is normally done well past the critical early-postnatal period; so their measurements show nothing about associations of developmental outcomes with exposures that take place during the developmentally most vulnerable postnatal period.
There is an underlying tendency that could explain most of the above indications of failure to perceive evidence of harmful effects of postnatal exposures. There appears to be a bandwagon effect, a prevailing belief that effects of postnatal exposures are very minor compared with effects of prenatal exposures. Many people’s minds are closed to evidence of effects of postnatal exposures. Some indication of that can be seen in the charts below, together with the accompanying statements of the authors of the study in which those charts appeared.
On the left are major sections of Figures 1 and 2 from a 2010 study (Davidson et al.44), consolidated here. Results are shown for a number of different tests administered to children who had varying levels of postnatal mercury. The authors acknowledged what is obvious in these charts by saying, “we did find significant adverse associations between recent postnatal MeHg (methylmercury) hair level and outcomes” in boys. But beyond that they said little more than that the gender effects were “intriguing,” that their “findings are sporadic and not consistent,”(!) and that “this outcome does not constitute evidence of any pattern of associations between MeHg and achievement.”
Bearing in mind that these charts show the results of all of the tests in which male and female scores were shown separately, one might wonder what it takes to qualify as “consistent” or “evidence of a pattern.” If these results had shown associations that were compatible with the general groupthink belief, rather than contrary to it, the authors’ descriptions of the results would probably have been quite different.
Most people (including scientists) will seldom look at studies sufficiently closely to see contradictions such as can be seen here. So the prevailing belief continues to prevail, without good reason.
For much more on the subject of effects of postnatal exposures to toxins, see www.autism-research.net/postnatal-effects.htm.
Section 3: Sources of fine particulate matter (PM-2.5) that are also sources of mercury, PCBs and PBDEs: Combustion of fossil fuels
Section 3.a: Sources of fine particulate matter:
According to a World Bank Group publication, “Almost all fine particulates are generated as a result of combustion processes, including the burning of fossil fuels …. In cold and temperate parts of the world, domestic coal burning has been a major contributor to the particulate content of urban air.”45 An EPA fact sheet goes into additional detail saying, “Sources of fine particle pollution (or the gases that contribute to fine particle formation) include power plants, gasoline and diesel engines, wood combustion, high-temperature industrial processes such as smelters and steel mills, and forest fires.”46 (underlining added) In the U.K., road transport exhaust and residential combustion have been found to be the first and second leading sources of PM-2.5; but in the rest of Europe, residential combustion as a source was reported to be more than twice as high as in the U.K., which was considered to probably stem from greater use of solid fuels (presumably mainly wood and coal).46
A Government of Canada (Environment Canada) web page indicates that home firewood burning was the source of about 40% of all fine particulate matter in Canada as of 2010. (not including emissions from natural sources and open sources such as road dust) Neighborhoods where such wood burning is widely done would probably be the areas most affected by the PM-2.5 emissions.47 Such a high percentage of total PM-2.5 from wood burning clearly does not apply in most of the U.S. (see chart below), but it probably has relevance in cold, northern parts of the U.S. where firewood is plentiful, such as Minnesota, Maine and Oregon (which states also, possibly not entirely by coincidence, have the highest rates of autism). In southern California, vehicular emissions have been found to be the largest source of PM-2.5, whereas in other parts of the state burning of biomass was found to be either the leading source or one of two equal leading sources.49
Above: Sources of Fine Particulate Matter in the U.S.
Section 3.b: Sources of mercury that are also sources of fine particulate matter:
After observing how Fossil Fuel Electricity Generators predominate as sources of PM-2.5 in the U.S. (chart above), note what the EPA reports elsewhere: “The largest identified source of mercury emissions during 1994-1995 is fossil fuel combustion, by utility boilers, particularly coal combustion.”50 The “Utility coal boilers” category was reported by the EPA to be the source of over half of all air emissions of mercury compounds in the U.S. in 2002.51
In short: Highest source of PM-2.5 = highest source of airborne mercury.
Observing in the above chart that wildfires are the third largest source of PM-2.5 in the U.S., also note that wildfires are also a very major source of airborne mercury: the Michigan Department of Environmental Quality explains this by saying, “This is due to the fact that forests act as mercury traps because mercury in the atmosphere collects on foliage.”52 A 2007 study estimated that mercury emissions from wildfires in the U.S. were about 44 metric tons per year.53 To better understand the significance of that many tons of mercury emitted to the U.S. air supply in one year, just from wildfires, note that the EPA has established a relatively safe level of mercury in air as 0.3 millionths of a gram per cubic meter,54 or about 8 billionths of an ounce per cubic yard of air.
As heavily present as mercury is (along with particulate matter) in coal combustion and wildfires, according to the EPA it also “exists naturally as a trace element in fossil fuels…. It is a highly volatile metal that vaporizes at the temperatures reached during the combustion zones….”(Section 4.1 of footnote 50) It would therefore be expected to be present also in diesel emissions, traffic-related pollution, and other combustion emissions; an Indian study found it to be even higher around traffic sites than around the industrial sites where measurements were taken.55
In short, again: Major source of PM-2.5 = major source of co-varying airborne mercury.
Section 3.c: Sources of PCBs and PBDEs, most of which are also sources of PM2.5:
Notice in the PM-2.5 chart (shown below again for convenient reference) and in the following text that the major sources of PM-2.5 are also major sources of PCBs: According to a web page of the NIH, PCBs are by-products from most forms of burning, including industrial burning, automobile exhaust, and wood or trash burning; the general category of toxins of which PCBs and PBDEs are well-known members (persistent organic pollutants) is emitted by “vehicle combustion engines, especially diesel engines;” wood, oil, coal, or biomass combustion, and blast furnaces or cement kilns.56 (italics added) (Be sure to note that wildfires, a major PM-2.5 source in the chart, are substantially combustion of biomass.)
Note in the above chart that Waste Disposal/Open Burning is a major source of PM-2.5; then note the following about backyard barrel burning (a common rural practice), which overlaps considerably with the Waste Disposal/Open Burning category: A 2003 paper by a team of five scientists, mainly from the EPA, studying emissions from backyard barrel burning, found that “total PCBs were approximately a factor of 200 greater than total PCDD/Fs (dioxins).”57 That would seem to indicate substantial emission of PCBs by backyard burning, especially since dioxin emissions from backyard barrel burning have been found by the EPA to be the greatest source of dioxins in the U.S. atmosphere as of the latest reports available, and a source of serious concern.57a
In short, yet again: Major source of PM-2.5 = major source of co-varying persistent neurodevelopmental toxins.
Notice what is shown in this EPA chart about PM2.5 emissions from diesel sources, in relation to emissions from gasoline-powered sources; it indicates that diesel nonroad emissions, which are not even shown in Figure 4, are over twice as great as the diesel onroad emissions that are shown to be very significant in that chart.
If nonroad and onroad diesel emissions were to be combined in that chart, the total category would be the second highest emission source of PM-2.5. (Nonroad diesel emissions, coming from locomotives, construction equipment, ships, and port and dredging equipment, would also be emitted near a substantial part of the population.) Remember from above the NIH statement that persistent organic pollutants (the category of which PCBs and PBDEs are important members) are especially high in diesel emissions. (See below for more specifics about that link.) It is relevant that three studies have found autism to be associated with exposures to atmospheric diesel emissions.58, 59, 60
In short, yet again: Varying concentrations of PM-2.5 in diesel emissions = similarly varying concentrations of persistent developmental toxins (including PCBs and PBDEs) in that same air.
Section 3.d: Diesel and urban sources of PCBs and PBDEs that are also sources of PM-2.5:
Having seen that diesel emissions (especially when including nonroad diesel emissions) are a very major source of fine particulate matter, note the following: According to a 2011 Taiwanese study, PBDEs (as well as PCBs) “exist in both gas and particle phases in the ambient air and stack flue gases” of heavy-duty diesel vehicles; the authors refer to three earlier studies, in addition to their own observations, as finding both PCBs and PBDEs in heavy-duty diesel emissions; and they note that higher-mileage vehicles emit larger quantities of both PCBs and PBDEs.61 (The California Air Resources Board estimates the life of heavy-duty trucks to be over 1,100,000 miles, indicating substantial use under conditions that emit larger quantities of PCBs and PBDEs.)62 In tests of five out of six diesel vehicles, PBDEs were present in the emissions in concentrations at least 50 times those of PCBs.63 A 2006 Spanish study, analyzing outdoor urban air, found that PBDEs in fine particulate matter (not merely in the same air space) were about ten times higher in mass than PCBs.64 PCBs have been a subject of major concern and study for a much longer period than PBDEs, and have been found to be a widespread urban atmospheric pollutant; 66 so it is very significant that a related toxin (PBDEs) has recently been found to be present in diesel emissions and in fine particulate matter in many-times greater concentrations than PCBs.
In short, yet again: Major sources of PM-2.5 (diesel vehicles and general urban air) = major sources of co-varying persistent neurodevelopmental toxins.
Section 4: Over five-fold differences in atmospheric PCB deposits according to distances from major roads -- PCBs are clearly an important component of particulate-containing air pollution.
In a 2013 U.S. study of PCB concentrations in carpet dust in homes at various distances from possible pollution sources, strong correlations were found between distances from major roads and PCB concentrations. In Los Angeles (the only location where these particular measurements were made), PCB concentrations were about five times as high in homes within 546 meters from major roads as they were in homes that were over 1000 meters from those roads.67 This finding has considerable relevance to the findings that autism has been associated with diesel emissions in at least three studies: Windham et al.,68 Volk et al., 2011,69 Roberts et al.70. In addition to those that found associations specifically with diesel emissions, also of relevance would be studies finding associations of autism with a general category that includes diesel emissions, such as Raz et al. and Kalkbrenner et al., 2015, with their findings of associations with particulate matter, and Volk et al., 2013, with its findings of associations with traffic related pollution.71
In short, yet again: Major source of PM-2.5 (vehicular combustion) = major source of co-varying persistent neurodevelopmental toxins.
-- Unlike particulate matter, PCBs are recognized by the EPA to be developmentally toxic. It is similar for mercury and PBDEs, other toxins that also typically accompany fine particulate matter.
One can go to the EPA’s web page, “Particulate Matter,” (http://epa.gov/ncer/science/pm) and search in vain for any words referring to neurological development or neurobehavioral effects. The opposite is true if one goes to the EPA’s web pages for health effects of PCBs (“Health Effects of PCBs”, at http://www.epa.gov/epawaste/hazard/tsd/pcbs/pubs/effects.htm, for mercury (http://www.epa.gov/mercury/effects.htm), and for PBDEs (http://www.epa.gov/oppt/existingchemicals/pubs/actionplans/pbde.html)
-- PCB exposures from air pollution reach the developing organism in minor doses prenatally, but in over-15-times-higher doses postnatally, via accumulation in the mother and subsequent excretion via lactation.
This was already stated earlier, with citations of authoritative sources (see Section 1.c), but it is so central to this discussion that it is worth repeating.
When studies find associations of autism with prenatal pollution exposures of the mother, they are also finding associations of autism with postnatal transfers to the infant of toxins that were accumulated prenatally. The main difference is that the postnatal doses are many times greater than the prenatal exposures, and those amplified postnatal exposures are received while the brain is still actively developing and vulnerable to toxins.
There is some debate about whether autism has actually been increasing, but there is excellent evidence that neurological disorders, of which autism is one, have been increasing. A 2008 publication of the U.S. Center for National Health Statistics reported as follows: “Over the past three decades in the United States, behavioral and learning disorders have emerged as major chronic conditions affecting the development of school-aged children and adolescents.” (This statement was based on observations of pediatricians and educators as well as government statistics.)75 Therefore, when studies find associations between air pollution and adverse neurological outcomes, and the latter have been increasing in recent decades, it is logical to consider what the trends have been like in air pollution.
Section 5.a: Air pollution has greatly declined while at the very same time neurological disorders “have emerged as major chronic conditions” among children.
If one does a Google search for “EPA trends in air pollution,” what one finds (in March of 2015), is four charts along the lines of the one below, all showing data for the same itemized pollutants, which are considered to be representative of air pollution in general. As is apparent below, air pollution has greatly declined during the period when child neurological disorders were greatly increasing.
The associations of neurological harm with air pollution (various kinds of air pollution as found in several different studies) are really compelling. But the opposite directions of the trends for neurological disorders and air pollution are a very serious contradiction of any idea of causality in those associations.
However, there is a perfectly logical explanation for how there could nevertheless be a causal connection in the associations of autism with air pollution, even with opposite trends. It has to do with the specific avenues by which toxins from the pollution reach the developing brain, either in very subdued form (placental transfer) or in greatly amplified doses (via breastfeeding). (see Sections 1.b and 1.c)
Section 5.b: Breastfeeding, the principal means of delivering neurodevelopmental toxins to the fetus/infant, has greatly increased while neurological disorders among children have “emerged” as major conditions.
There appear to be only four recognized or strongly suspected neurodevelopmental toxins that have been found to widely reach fetuses or infants in doses greatly exceeding established safe levels. Three of those (PCBs, mercury and PBDEs) are the three toxins dealt with earlier, all of which are known to accompany the particulate matter pollution that has been associated with autism. (see Section 3)
a) PBDEs, normally well above and up to 20 times the EPA’s RfD (reference dose, or relatively safe dose);75a
b) mercury, typically four times the maximum allowed by U.S. law in bottled water, but in many cases much higher than that;75b and
c) PCBs, in human milk in concentrations about 20 times the maximum allowed by law in U.S. public water supplies.75c
All three of the above are present in infant formula in concentrations less than 4% as high, and usually less than 1% as high, as their concentrations in human milk.75d
Letters were sent to seven scientists involved in the area of autism, asking if they were aware of any avenue of exposure other than breastfeeding by which developing brains are widely exposed to recognized developmental toxins in doses exceeding established safe doses; of the three replies received, none has suggested any such possible avenue.75e
Note in the chart below the specific years during which the long, major increase in breastfeeding rates in the U.S. began; then add five or six years after birth before the children would reach school age, and then notice how close that comes to 1978; three decades before 2008 (approx. 1978) was the approximate time when, according to a CDC report, certain neurological disorders reportedly “emerged as major chronic conditions affecting the development of school-aged children and adolescents.”75
Breastfeeding rates in the U.S. were low for over 25 years during the mid-20th century,77 until the increases took place that are shown in the charts above. The middle of the century was also a transitional period for exposures to toxins in industrialized societies; experts on the subject of environmental contaminants pointed out in 2004 that "these substances have caused contamination of human milk only during the last half century."78 Therefore, when the increases in breastfeeding rates began in the early 1970’s, that brought on a major increase in exposures of infants to developmental toxins: the recently increased levels of environmental toxins were combined for the first time with rapidly increasing transmission to infants of maternal accumulations of those toxins.
Given that the apparently predominant means of transferring developmental toxins to the developing brain in concentrated form has been greatly increasing, it is understandable that neurological disorders could be increasing even while the primary emissions of toxins in the atmosphere have been declining. It is entirely possible that air pollution’s toxic contents become seriously harmful mainly or even only after they become concentrated by the lactation process before being transferred to the developing infant in high doses.
By comparison, placental transfer of inhaled developmental toxins is minimal. (See Sections 1.b and 1.c)
Section 6: Evidence that postnatal exposures of the developing brain to toxins cause neurodevelopmental disorders
Section 6.a On the basis of data from all 50 states and 51 U.S. counties, a highly-published scientist and Fellow of the American College of Nutrition (R.J. Shamberger) found that "exclusive breast-feeding shows a direct epidemiological relationship to autism" and also that "the longer the duration of exclusive breast-feeding, the greater the correlation with autism."79 Another U.S. study, a U.K. study and a Canadian study all arrived at compatible findings.80
Section 6.b PCBs: A large team of German scientists and doctors, studying 171 healthy mother-infant pairs, found "negative associations between (human) milk PCB and mental/motor development ... at all ages, becoming significant from 30 months onwards." In addition, "negative associations with PCB increased with age." 81 Also according to a German scientist, “Several prospective cohort studies - including our Düsseldorf study - have demonstrated that pre- and early postnatal exposure to PCBs is associated with deficit or retardation of mental and/or motor development.” 82
PBDEs: A 2011 study found that 4-year-olds with higher levels of PBDEs had over 2½ times the risk of poor social competence (a trait that is central to ASD), compared with children with lower levels of PBDEs;83 this should be seen in combination with the nearly 3-to-1 difference in levels of PBDEs in breastfed as compared with formula-fed children at age 4, as reported in what is apparently the only study that has made such a comparison.84
Mercury: At least five published studies have found high levels of mercury in those with autism.85 The studies finding associations of autism with mercury levels less than twice the normal range should be seen together with the findings in multiple studies of doubling or tripling of infant mercury levels in association with extended breastfeeding versus no breastfeeding, taking place during the infant’s period of rapid brain growth.86
For much more evidence on this general subject, see www.autism-correlatons.info.
Section 6.c Studies linking autism with atmospheric pollution, especially with postnatal exposures:
The Raz et al. study has already been discussed extensively above.
The 2013 Volk et al. study found a far higher odds ratio for postnatal exposures than the odds ratios that were found for prenatal exposures in any of the three studies being discussed here. This study found an odds ratio of 3.1 for residence during the first year of life in areas in the top quartile of traffic-related pollution, compared with controls.87
The 2015 Kalkbrenner et al. study.88 Notice in this chart from that study, below, that the period of highest odds in the entire chart for an association between autism and PM exposure was in the third postnatal quarter, in California.
Also note that the third highest odds ratio in the entire chart is the first postnatal quarter in North Carolina. So, of the three periods (by state) with the highest odds ratios for autism association with PM, two of the three were postnatal.
The high postnatal odds in the first quarter in North Carolina are compatible with the period of rapid brain development, therefore vulnerability to toxins, that occurs in the early weeks after birth; (see Section 2.a) that is also the time when toxins that have been accumulating during the late months of gestation are being mobilized from the fat tissues and reaching the developing infant in concentrated form. (see Section 1.c)
The especially high odds in the third postnatal quarter in California is in agreement with the very high postnatal odds found in California in the Volk et al. study (above); and both are probably related to the fact that breastfeeding of long duration (and therefore more extensive transfer of toxins to the infant) is unusually high in California; breastfeeding for 12 months or more is over twice as high in California as in North Carolina and also 40% higher than the U.S. average. 89 Relevant to the high percentage of extended breastfeeding in California and the very strong association of autism there with postnatal exposure to traffic pollution, remember the following from Section 2:
(a) considerable development of the brain (therefore vulnerability to toxins) takes place for more than a year after birth,
(b) infants breastfed for a year have been found to have three times the mercury levels compared with formula-fed infants (see mercury above),
(c) children breastfed for 6 to 12 months were found in a 2014 study to have over nine times the PCB levels compared with formula-fed children even at age 3½;38 and
(d) those recognized developmental toxins (mercury and PCBs) are emitted by the same sources that emit particulate matter (see Section 3 above)
In addition to the above evidence of high odds for increased autism with elevated postnatal PM exposure in the two states separately, there was at least one period when the postnatal odds of increased autism were very high for the combined data for the two states; in fact, this postnatal odds ratio was about 50% higher than the highest of the prenatal odds ratios that were found. That became apparent by means of a more precise examination of the data, as shown in another chart from the Kalkbrenner study, below. The chart as shown below has been modified in a few minor ways to make it easier to perceive some relevant points, as follows:
a) the vertical orange line was inserted at the average day of birth, the number of days after conception by which time the average birth had already taken place; (this was determined by where the Cases Born and Controls Born lines cross the 50% line);
b) the orange and blue arrows were inserted to refer to important segments of the data, which will be explained below.
The authors refer to this chart as a way of depicting the post-conception time periods in which “higher autism risk corresponded with short windows of PM10 exposure.” Increased odds during late gestation, compared with early gestation, are obvious in the chart. The authors also referred to “stronger associations around the time of birth,” and that presumably refers at least in part to the brief period with the chart’s very highest odds ratio for autism in relation to PM exposure, toward which the orange arrow points; notice that this time of maximum risk occurred after the average time of birth. Although that peak appears to be very brief, note that the authors estimated odds ratios by 14-day periods, so this peak could apply to a period extending for two weeks or more after birth. The first postnatal peak was followed by a sharp drop in the odds ratio, but that drop was in turn followed by a second steep postnatal increase (see blue arrow). Unfortunately, only the upper confidence line is shown for the second increase that is taking place after the average birth, and the chart ends there. (The upper confidence line indicates that there is a 1 out of 20 chance that the actual correct value for the odds ratio would be at that height.) In any case it is worth emphasizing that, by a wide margin, the highest odds ratio of autism in relation to PM exposure (based on the results of the complete study) was found to be after birth.
Even though relatively brief, that postnatal period of highest odds for autism may well be the time when most of the damage to developing brains occurs. The longer duration of the prenatal period of increased odds ratios is perfectly compatible with that being the time when the mother is inhaling toxins that will be accumulating in her body (see Section 1.d), forming deposits in adipose tissue that will be mobilized after birth and transferred to the infant in concentrated form via breast milk. (see Section 1.c) Remember that most of the particulate matter and accompanying toxins inhaled by the mother do not cross the placental barrier (see Section 1.b. and 1.c); and the brain’s prenatal development is less vulnerable to toxin-induced hypothyroidism, due to presence of the mother’s thyroid hormones. (see Section 2.a, item 3)
By contrast, the early days after birth are a period when atmospheric toxins that are newly inhaled by the mother are being added to the mother’s accumulations of toxins from earlier exposures, and the combination enters breast milk and is ingested by breastfed infants.11 This represents a sharp increase in the developing organism’s exposure to effects of atmospheric toxins, since the fetus receives only the minor percentages of prenatal exposures that can get through the placental barrier (see Sections 1.b and 1.c). Remember the expert statement, "Significantly more (10 to 20 times) of a mother's body burden of persistent organohalogens is transferred to the infant via the milk than by the transplacental route." 11 (Organohalogens are developmental toxins such as are typically emitted by the same sources that emit PM-2.5 -- see Section 3)
This combined, greatly increased, direct exposure takes place during the window of susceptibility to neonatal hypothyroidism, which the NIH says can lead to intellectual disability. And the NIH lists many traits of intellectual disability that have great similarities to characteristics of autism. (see Section 2.a, item 3)
Section 7: Bringing together findings from the three related 2013-2015 studies.
Two out of three studies found the greatest associations of autism with postnatal exposures of the infant, and the third study did not conflict with the possibility of a strong but brief postnatal effect.
The three studies dealt with above have investigated odds ratios of autism in relation to selected time periods of increased or decreased exposure to atmospheric toxins. Two of those three (Volk et al. 201387 and Kalkbrenner et al. 201589a) found that the highest odds ratios for autism in relation to toxin exposures were during the year after birth. The third study, Raz et al.,1 did not arrive at that finding, but its failure to do so is very likely related to the lengthy time period over which its postnatal data was averaged (9 months); an effect that is very strong but of brief duration (such as actually occurred -- see Section 6.e) could become insignificant after being averaged in with considerable other data from an entire 9-month period. Also, since this study investigated a population of nurses, its data probably applied mainly to mother-infant pairs with relatively short durations of breastfeeding; based on three studies, there are good reasons (including compatibility with continued work) to suspect that nurses are likely to breastfeed for shorter durations than the general population. (see Appendix C) Therefore toxins transmitted during breastfeeding by those mothers would more closely represent the accumulations that were acquired before birth, with less effect from postnatal exposures to atmospheric toxins.
The strong association of traffic pollution with autism when measured postnatally should not be surprising:
As mentioned, an especially high odds ratio for autism was found in relation to postnatal exposures to atmospheric toxins, in the Volk et al. California study. Notice the outstandingly-high ratio for association of mixed traffic pollution with autism in that study's results as shown on the bottom line in the chart below:
The "Yr 1" just above the bottom line of the chart indicates that exposure to traffic pollution was measured postnatally in the Volk et al. 2013 study,87 compared with the prenatal times of measurement that applied to all of the other studies in that "Mixed Traffic" grouping. Notice how outstandingly high the effect of the postnatal exposure appears to be compared with effects of the prenatal exposures.
There are good reasons why the apparent effects of postnatal exposures should be much worse than effects of prenatal exposures: During the year after birth, air pollution would be inhaled by adult-size lungs of breastfeeding mothers, and pollutants would then be transferred in concentrated form to the infant (see Section 1.c) , without obstruction by the placental barrier as occurs prenatally.
When studies find associations of autism with prenatal exposures of the mother to pollution, they are also finding associations of autism with postnatal transfers to the infant of toxins that were accumulated outside the fetus before birth. The main difference is that the postnatal doses are many times greater than the prenatal exposures, and those amplified postnatal exposures are received while the brain is still actively developing and vulnerable to toxins.
The postnatal, greatly-increased ingestion of accumulated toxins should therefore be of the greatest concern. That is especially true since the postnatal ingestions, unlike the prenatal exposures, can be rapidly and greatly reduced. Most cows do not have major exposures to the combustion emissions, including traffic emissions and urban air, that are sources of particulate matter and its accompanying toxins. The rarely-breastfed mid-20th-century generation did not have health problems that have become common since then.
Comments or questions on the above are invited, including criticisms if they are specific, and will usually receive a response. At the next link are past comments and questions from a number of readers, including eight doctors, followed by our responses. Some of the doctors have been critical but others have been substantially in agreement with us (including one with children with asthma, one who says she has delivered thousands of babies, and one with a son with autism); they put into briefer, everyday language and personal terms some important points that tend to be immersed in detail when presented in our own publications. Topics discussed in that section include about having breast milk tested for toxins and about means of trying to achieve milk that is relatively free of toxins, including the “pump and dump” option. To read the above, go to www.pollutionaction.org/comments.htm
In criticisms, please point out any specific passages that you feel are not accurately based on authoritative sources (as cited) or that do not logically follow from the evidence presented. Note that the author of this article feels no obligation to present the pro-breastfeeding case as long as the medical associations and other promoters of breastfeeding fail to inform parents about the developmental toxins that are, without dispute, present in high concentrations in human milk. Please e-mail to email@example.com.
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 firstname.lastname@example.org. 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
Appendix A: Especially rapid transfer of toxins after birth compared with minimal exposures before birth:
PCBs and PBDEs:
-- A Dutch cohort study of over 400 mother-infant pairs, as summarized by a team of three American scientists, reported that cord plasma levels of PCBs were one-fourth to one-fifth the levels in maternal plasma PCBs;92
-- a 2008 study by eight Japanese scientists found that PBDEs were about 30 times as high in breast milk as in cord blood.93
-- In a study of both occupationally-exposed and non-exposed women, it was found that PCB levels in the newborns were 1/10th to 1/20th of the mother’s levels (relative to body weight).94
-- According to the experts on neurological development , P. Grandjean and PJ Landrigan, in a 2006 article, “Persistent lipophilic substances, including specific pesticides and halogenated industrial compounds, such as PCBs, accumulate in maternal adipose tissue and are passed on to the infant via breast milk, resulting in infant exposure that exceeds the mother’s own exposure by 100-fold on the basis of bodyweight.”96 (Note that halogenated compounds also include PBDEs) When a very similar statement was again made in a 2013 study to which Raz et al. respectfully refer,97 no reference was cited to support that statement, implying that the three scientist-authors and their peer reviewers considered the substance of that statement to be sufficiently well known and undisputed in the scientific community that there was no need for a reference.
-- Those high early-postnatal doses of most of these toxins are apparently well absorbed by infants, whereas the fetus apparently receives some protection provided by the placenta. In an experiment with mice, it was found that 5-week-old offspring contained 100 or more times as much PCBs as were contained in the fetus, and most of that had been transferred by lactation.98
-- A Japanese study of human infants found that PCB levels in the blood of breast-fed children increased “markedly” after birth; but even with such sharp increases right after birth, it was still three months before the infants’ PCB levels reached those of their mothers. (By contrast, PCB blood levels in bottle-fed children declined after birth.)99 Considering that infants’ PCB levels increased “markedly” after birth, yet it still took three months before the infants’ blood levels reached those of their mothers, this is good additional evidence that fetal exposure (to recognized toxins) is likely to be quite minimal.
-- In an American study, investigating children of mothers who had consumed large amounts of Great Lakes fish, body burden of PCBs in children breastfed for at least 6 months was found to be about 17 times as high as the burdens of those who had not been breastfed (5.1 vs. 0.3 ng/ml)100
Aside from the evidence about mercury exposures indicated in Section 2.b, note the following:
-- Animal studies have demonstrated that mercury from mercury vapor exposure is excreted into milk.
-- Human studies indicate that about 70%-85% of inhaled mercury vapor is absorbed by the lungs into the bloodstream.101
-- Another study with humans and an experiment with monkeys provide still more confirmation that, for most infants, fetal exposures to developmental toxins to which the mother is exposed are small, especially compared with the exposures to those same toxins that come after birth via lactation.102
Appendix B: Causes and effects of neonatal hypothyroidism
According to an article in an Oxford Journal, “Mental retardation resulting from neonatal thyroid hormone deficiency is an example of a disorder in which subtle changes in neural circuitry are associated with devastating functional consequences…. TH deficiency also causes specific defects in cell migration.”103 According to a highly-published Japanese expert on this subject, in a 2008 study, “thyroid hormone plays a crucial role in cerebellar development. Deficiency of thyroid hormone results in abnormal cerebellar growth and differentiation…. the expression of many thyroid-hormone-responsive genes is altered by thyroid hormone status only during early postnatal critical period.” 104 A 2008 EPA research report notes that “hypothyroidism during fetal and early neonatal life may have profound adverse effects on the developing brain.”105
Even if thyroid deficiency is not sufficiently serious to cause severe consequences, the effects can still be substantial. According to an American/Canadian pair of scientists in an article in the Journal of Endocrinology, even if neonatal hypothyroidism is detected and treated (there is normally one screening for it in newborns in the U.S.), “these children still exhibit impairments…. Their IQ levels average approximately 6 points below expectation and they also show selective deficits on visuospatial, motor, language, memory and attention tests. Approximately 20% of cases also have a mild sensorineural hearing loss, which contributes to difficulties in initially learning to read.”106 In a review of seven studies by Dutch scientists, the authors concluded that hypothyroidism, “despite early detection and treatment, results in an IQ deficit.”107 When reading about the above effects of neonatal low thyroid (as well as those from the NIH to follow), think of their similarities to frequent traits of children with autism and/or ADHD. And note that those harmful effects are likely even if the outcomes are improved as a result of the low thyroid levels’ being detected and treated. It is important to note that the outcome could well be worse than that improved outcome; an article in the journal of the American Academy of Pediatrics recognizes that low thyroid levels can come about after the newborn screening and can very possibly go undetected,108 while the brain’s development is being damaged.
According to a study by Spanish and French scientists, published in 1995 in the European Journal of Endocrinology, “Thyroid hormone deficiency … impairs the cytoarchitecture of the neocortex and the cerebellum,” altering patterns of lamination, cell migration and formation of connections. Formation of connections in the cerebellum, specifically, “is decreased markedly” in association with low thyroid.109 Note that important parts of the neocortex and most of the cerebellum develop in the early postnatal period.110 Also note that improper cell migration, formation of connections, and other organizational processes (all of which take place postnatally, either partly or predominantly)111 have been implicated with autism.112
A German-American team of four scientists found in a 1999 study that five different forms of PCBs were significantly negatively associated with thyroid hormone levels in 7-to-10-year-old children.115
A Dutch study of 418 mother-infant pairs found that prenatal exposure to dioxins and PCBs did not show a correlation with postnatal neurological optimality, whereas “only breast-fed children who were perinatally exposed to higher dioxin, mono-ortho PCB, di-ortho PCB and total PCB/dioxin TEQ values showed a reduced neonatal neurological optimality.”116 To read about 16 other studies that found postnatal exposures to toxins to have greater harmful neurodevelopmental effects than prenatal exposures to the same toxins, see Section 3, cont. of www.autism-research.net/postnatal-effects.htm)
Appendix C: Short duration of breastfeeding by mothers studied by Raz et al.?
Nurses, the group whose data were used in the Raz et al. study, may well have shorter than average durations of breastfeeding, which would tend to cause the effects of their breastfeeding to be mainly close to the time of birth. Being in a healthcare profession, they would be likely to at least initially follow the general medical recommendations to breastfeed their infants, but their working lives would very often not be conducive to long-term breastfeeding. In an article in a publication of the American Nurses Association, it is stated, “Barriers identified by working mothers include inflexible working hours, lack of privacy and location to express milk, having no place to store expressed milk, concerned about job security, and have limited maternity leave benefits… Many mothers encounter pressure from supervisor and coworkers not to take breaks to express milk.”117 These comments were about workplaces in general, but the Nurses Association said nothing about any healthcare facilities’ setting good examples in any of the problem areas mentioned. In a study of “findings from an Australian health service workplace,” it is stated that there was “little perceived support from the organisation (13%) and human resources (6%). Most women (92%) had received no information from their managers about their breastfeeding options upon their return to work, and few had access to a room specially designated for breastfeeding.” Other problems were lack of flexible work options and lactation breaks.118 Another study summarized findings of previous studies (in Malaysia and Nigeria) as follows: “Exclusive breastfeeding among health professional women is very low….The major reason mentioned by the respondents for termination of breastfeeding was employment;” the authors then reported similar findings of their own study, in Ethiopia.119 Specifically, they found that “The odds of exclusive breastfeeding practice by the respondents who were midwives by profession were two times higher compared with nurses;” it is likely that the midwives were more representative of the general population, providing an indication of how low exclusive breastfeeding was found to be among nurses, by comparison.
1) Raz et al., Autism Spectrum Disorder and Particulate Matter Air Pollution before, during, and after Pregnancy: A Nested Case–Control Analysis within the Nurses’ Health Study II Cohort, Environ Health Perspect; Volume 123 | Issue 3 | March 2015 DOI:10.1289/ehp.1408133 at http://ehp.niehs.nih.gov/1408133
2) Kalkbrenner et al., Particulate matter exposure, prenatal and postnatal windows of susceptibility, and autism spectrum disorders, 2015 Jan;26(1):30-42. doi: 10.1097/EDE.0000000000000173. at http://www.ncbi.nlm.nih.gov/pubmed/25286049
4) Masuda et al., Transfer of polychlorinated biphenyls from mothers to foetuses and infants, Food and Cosmetics Toxicology, Volume 16, Issue 6, December 1978, Pages 543–546, at http://www.sciencedirect.com/science/article/pii/S0015626478802211 PCBs are a pollutant that is normally together with the PM2.5 emissions that were studied in the Raz et al. study; this study by nine Japanese scientists collected blood and other tissues of mothers and stillborn fetuses and analyzed it for PCBs, and found indications that “there may be a placental barrier against PCBs.”
7a) Wick et al., Barrier Capacity of Human Placenta for Nanosized Materials, Environ Health Perspect. 2010 Mar; 118(3): 432–436, Published online 2009 Nov 12. doi: 10.1289/ehp.0901200 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854775/
8) EPA web page at http://www2.epa.gov/international-cooperation/persistent-organic-pollutants-global-issue-global-response, and many other sources can be provided on this on request.
9) Guvenius et al., Human prenatal and postnatal exposure to polybrominated diphenyl ethers, polychlorinated biphenyls, polychlorobiphenylols, and pentachlorophenol, Environ Health Perspect. 2003 Jul; 111(9): 1235–1241. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241580, Showing concentrations of PCBs and PBDEs in breast milk being about 16 times as high as in cord blood plasma.
10) Koopman-Esseboom et al. 1994a. PCB and dioxin levels in plasma and human milk of 418 Dutch women and their infants. Predictive value of PCB congener levels in maternal plasma for fetal and infant’s exposure to PCBs and dioxins. Chemosphere 28:1721–1732, at http://repub.eur.nl/pub/59878
11) Jensen, A.A. et al, Chemical Contaminants in Human Milk, CRC Press, Inc., Boca Raton, Ann Arbor, Boston, 1991, p 15. Findings of above confirmed in animal tests, with even greater contrasts, in Ahlborg et al., Risk Assessment of Polychlorinated Biphenyls (PCBs), Nordic Council of Ministers, Copenhagen. Report NORD 1992; 26
Also see www.breastfeeding-toxins.info.
12) “The intestinal absorption of PCB in a breast-fed infant was more than 95%”, WHO Regional Office for Europe, Air Quality Guidelines, Second Ed., 2000: Ch. 5.10: PCBs, p. 11 at http://www.euro.who.int/__data/assets/pdf_file/0016/123064/AQG2ndEd_5_10PCBs.PDF
13) 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 184.108.40.206, at www.epa.gov/raf/publications/pdfs/PPKFINAL.PDF
14) Harrad et al., Concentrations of polychlorinated biphenyls in indoor air and polybrominated diphenyl ethers in indoor air and dust in Birmingham, United Kingdom: implications for human exposure. Environ Sci Technol 2006; 40: 4633–8.
15) NIH web page at http://hazmap.nlm.nih.gov/category-details?id=1954&table=copytblagents
16) Thuresson et al.,Apparent Half-Lives of Hepta- to Decabrominated Diphenyl Ethers in Human Serum as Determined in Occupationally Exposed Workers, Environ Health Perspect. 2006 Feb; 114(2): 176–181, Published online 2005 Sep 21, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1367828/
16a) 0ab) Danish Health and Medicines Authority, 2013, Health risks of PCB in the indoor climate in Denmark, at http://sundhedsstyrelsen.dk/publ/Publ2013/12dec/HAofPCBindoorDK_en.pdf. p. 90
17) U.S. Dept. of Energy, Risk Assessment Information System: C.B. Bast, Formal Toxicity Summary for AROCLOR-1260 at http://rais.ornl.gov/tox/profiles/aroclor_1260_f_V1.html
18) ATSDR publication at http://www.atsdr.cdc.gov/sites/toxzine/mercury_toxzine.html
-NIH website on endocrine disruptors at www.niehs.nih.gov/health/topics/agents/endocrine
--Section 6.4.2 of Mercury Study Report to Congress c7o032-1-1, Office of Air Quality Planning & Standards and Office of Research and Development Volume VII at http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf
19) Rice et al., Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models, EPA National Center for Environmental Assessment, at www.ncbi.nlm.nih.gov/pmc/articles/PMC1637807, p. 515. According to these EPA researchers, studies “have clearly demonstrated that when proliferation is actively occurring in a given region of the brain, it is vulnerable” to toxins.
20) National Research Council (U.S.). Committee on Toxicology, Recommendations for the Prevention of Lead Poisoning in Children, p. 19, at https://books.google.com
21) Myers et al., Postnatal Exposure to Methyl Mercury from Fish Consumption: a Review and New Data from the Seychelles Child Development Study, Neurotoxicology. May 2009; 30(3): 338–349. Published online Jan 21, 2009. doi: 10.1016/j.neuro.2009.01.005 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2743883 Also see footnote 5c above.
24) Rice et al., Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models, EPA National Center for Environmental Assessment, at www.ncbi.nlm.nih.gov/pmc/articles/PMC1637807
25) Holland et al., Structural growth trajectories and rates of change in the first 3 months of infant brain development, 2014 Oct;71(10):1266-74. doi: 10.1001/jamaneurol.2014.1638. at http://www.ncbi.nlm.nih.gov/pubmed/25111045
26) Huppi et al., Quantitative magnetic resonance imaging of brain development in premature and mature newborns, 1998 Feb;43(2):224-35. at http://www.ncbi.nlm.nih.gov/pubmed/9485064
27) Tau et al., Normal Development of Brain Circuits, Neuropsychopharmacology. Jan 2010; 35(1): 147–168. Published online Sep 30, 2009. doi: 10.1038/npp.2009.115 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055433/
30) NIH web page at http://www.nlm.nih.gov/medlineplus/ency/article/001193.htm Also see EPA statement at U.S. EPA: Toxicological Review of 2,2',4,4'-Tetrabromodiphenyl Ether (BDE-47) EPA/635/R-07/005F www.epa.gov/iris, p. 40 at http://www.epa.gov/iris/toxreviews/1010tr.pdf
31) A seven-scientist team of French researchers stated in a 2010 study that “TH (thyroid hormone) plays an important role in cerebellar neurogenesis, a mainly postnatal developmental process… perinatal hypothyroidism (leads to) a striking reduction in the growth and branching” of connections in the developing brain. (Boukhtouche et al., Induction of early Purkinje cell dendritic differentiation by thyroid hormone requires RORα, Neural Development 2010, 5:18 doi:10.1186/1749-8104-5-18 at http://www.neuraldevelopment.com/content/5/1/18) In a 2000 article in the journal Cerebral Cortex, an Oxford Journal, it is stated that “neonatal TH deficiency severely impacts development…. Mental retardation resulting from neonatal thyroid hormone deficiency is an example….” 103 (italics added)
32) Drexler et al., The mercury concentration in breast milk resulting from amalgam fillings and dietary habits, Environ Res. 1998 May;77(2):124-9. at http://www.ncbi.nlm.nih.gov/pubmed/9600805. another study also found evidence of excretion of mercury during breastfeeding. (Vahter, 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
33) Jugo, Metabolism of toxic heavy metals in growing organisms: A review Environmental Research, Vol. 13, Issue 1, February 1977, Pages 36–46, at http://www.sciencedirect.com/science/article/pii/0013935177900020
34) U.S. ATSDR: Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000 at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf, pp. 21, 18 The ATSDR refers to “extensively corroborated findings in experimental animals that exposure to PCBs in utero and/or during early development (e.g., through breast milk) can deplete levels of circulating thyroid hormones in the fetus or neonate, which may give rise to a hypothyroid state during development.” The Danish Health and Medicines Authority says essentially the same thing except that they indicate greater certainty about the expected result of low thyroid. (Danish Health and Medicines Authority, 2013, Health risks of PCB in the indoor climate in Denmark, at http://sundhedsstyrelsen.dk/publ/Publ2013/12dec/HAofPCBindoorDK_en.pdf)
35) Developmental Neurotoxicity of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Costa et al., Neurotoxicology. 2007 November; 28(6): 1047–1067. doi: 10.1016/j.neuro.2007.08.007 PMCID: PMC2118052 NIHMSID: NIHMS34875 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052/
See also U.S. ATSDR, Polybrominated Biphenyls (PBBs) & Polybrominated Diphenyl Ethers (PBDEs), Section 4, p. 41 at http://www.atsdr.cdc.gov/ToxProfiles/tp.asp?id=529&tid=94
36) Koopman-Esseboom et al., Effects of dioxins and polychlorinated biphenyls on thyroid hormone status of pregnant women and their infants, Pediatr Res. 1994 Oct;36(4):468-73. at http://www.ncbi.nlm.nih.gov/pubmed/7816522
37) Turyk et al., Relationships of Thyroid Hormones with Polychlorinated Biphenyls, Dioxins, Furans, and DDE in Adults, Published online May 31, 2007. doi: 10.1289/ehp.10179 at www.ncbi.nlm.nih.gov/pmc/articles/PMC1940071/
38) Jusko et al., Prenatal and Postnatal Serum PCB Concentrations and Cochlear Function in Children at 45 Months of Age, Environmental Health Perspectives, 22 July 2014 (Advance Pub.) at http://ehp.niehs.nih.gov/wp-content/uploads/advpub/2014/7/ehp.1307473.pdf
39) NIH web page at http://www.nlm.nih.gov/medlineplus/ency/article/001523.htm
40) Philippe Grandjean, in “Neurodevelopmental Disorders” in Children’s Health and Environment: A Review of Evidence, published by WHO, Regional Office for Europe, at www.euro.who.int/__data/assets/pdf_file/0007/98251/E75518.pdf p. 67 Also, P. Grandjean, Methylmercury Exposure Biomarkers as Indicators of Neurotoxicity in Children Aged 7 Years, American Journal of Epidemiology 1999, The Johns Hopkins University School of Hygiene and Public Health at http://aje.oxfordjournals.org/content/150/3/301.full.pdf : “The nervous system is particularly vulnerable to effects from neurotoxicants such as methylmercury during the last two trimesters of pregnancy and during early postnatal life.”
-- Rodier, “Developing Brain as a Target of Toxicity,” Environmental Health Perspectives, at www.ncbi.nlm.nih.gov/pmc/articles/PMC1518932/pdf/envhper00365-0077.pdf Also see Rice et al., Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models, EPA National Center for Environmental Assessment, at www.ncbi.nlm.nih.gov/pmc/articles/PMC1637807, p. 515.
-- ATSDR publication at http://www.atsdr.cdc.gov/sites/toxzine/mercury_toxzine.html
-- NIH website on endocrine disruptors at www.niehs.nih.gov/health/topics/agents/endocrine
-- EPA: Section 6.4.2 of Mercury Study Report to Congress c7o032-1-1, Office of Air Quality Planning & Standards and Office of Research and Development Volume VII at http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf Also U.S. EPA: Toxicological Review of 2,2',4,4'-Tetrabromodiphenyl Ether (BDE-47) EPA/635/R-07/005F www.epa.gov/iris, p. 40 at http://www.epa.gov/iris/toxreviews/1010tr.pdf
44) Davidson et al., Fish Consumption, Mercury Exposure, and Their Associations with Scholastic Achievement in the Seychelles Child Development Study, Neurotoxicology. Author manuscript; available in PMC Sep 1, 2011, Published in final edited form as:Neurotoxicology. Sep 2010; 31(5): 439–447. Published online May 31, 2010. doi: 10.1016/j.neuro.2010.05.010, PMCID: PMC2934742 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2934742/
45) World Bank Group, Pollution Prevention and Abatement Handbook, Airborne Particulate Matter, 1998, at http://www.ifc.org/wps/wcm/connect/59cfb38048855493b35cf36a6515bb18/HandbookAirborneParticularMatter.pdf?MOD=AJPERES
46) EPA: Fact Sheet: Final Revisions to the National Ambient Air Quality Standards
for Particle Pollution (Particulate Matter), at http://www.epa.gov/airquality/particlepollution/pdfs/20060921_factsheet.pdf
47) Government of Canada, Environment Canada: Particulate Matter Emissions, at http://www.ec.gc.ca/indicateurs-indicators/default.asp?lang=en&n=52F0AE93-1
49) Hasheminassab et al., Spatial and temporal variability of sources of ambient fine particulate matter (PM2.5) in California, Atmos. Chem. Phys., 14, 12085–12097, 2014, www.atmos-chem-phys.net/14/12085/2014/ doi:10.5194/acp-14-12085-2014 at http://www.atmos-chem-phys.net/14/12085/2014/acp-14-12085-2014.pdf
50) U.S. EPA, Mercury Study, Report to Congress, c7o032-1-1, Volume II: An Inventory of Anthropogenic Mercury Emissions in the United States, p. 5-7, at http://www.epa.gov/ttn/oarpg/t3/reports/volume2.pdf
51) EPA: 2002 Air Quality Emissions Data Analysis Booklet at http://www.epa.gov/ttnchie1/net/2002neibooklet.pdf
52) (State of) Michigan DEQ MERCURY STRATEGY STAFF REPORT, p. 34, at http://www.michigan.gov/documents/deq/MDEQ_MSWG_FinalReportJan2008.pdf_222256_7.pdf
53) Wiedenmyer et al., Mercury Emission Estimates from Fires: An Initial Inventory for the United States” Environ. Sci. Technol. 2007, 41, 8092–8098, at http://pubs.acs.org/doi/pdfplus/10.1021/es071289o
55) Table 4 of Singh et al., Quantifying uncertainty in measurement of mercury in suspended particulate matter by cold vapor technique using atomic absorption spectrometry with hydride generator, Springerplus. 2013; 2: 453. doi: 10.1186/2193-1801-2-453 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3786082/
56) U.S. National Library of Medicine, Toxtown, Persistent Organic Pollutants (POPs), at http://toxtown.nlm.nih.gov/text_version/chemicals.php?id=86
57) Lemieux et all., Variables Affecting Emissions of PCDD/Fs from Uncontrolled Combustion of Household Waste in Barrels, Journal of the Air & Waste Management Association, 2012, at http://www.tandfonline.com/doi/pdf/10.1080/10473289.2003.10466192
57a) EPA: An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000, EPA/600/P-03/002F November 2006, Table 1-17, at www.epa.gov/ncea/pdfs/dioxin/2006/dioxin.pdf
58) Volk et al., Residential proximity to freeways and autism in the CHARGE study. Environ Health Perspect 119:873–877, 2011
59) Windham et al., 2006. Autism spectrum disorders in relation to distribution of hazardous air pollutants in the San Francisco Bay area. Environ Health Perspect 114:1438–1444
60) Roberts et al., Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ Health Study II Participants, Children's Health Volume 121 | Issue 8 | August 2013, Environ Health Perspect; DOI:10.1289/ehp.1206187 at http://ehp.niehs.nih.gov/1206187/#r35
61) Lien-Te Hsieh et al., Reduction of Toxic Pollutants Emitted from Heavy-duty Diesel Vehicles by Deploying Diesel Particulate Filters, Aerosol and Air Quality Research, 11: 709–715, 2011 ISSN: 1680-8584 print / 2071-1409 online doi: 10.4209/aaqr.2011.05.0058 at http://aaqr.org/VOL11_No6_November2011/8_AAQR-11-05-OA-0058_709-715.pdf
62) California ARB, "Emissions Inventory," Section 34, showing 290,000 miles to be 25% of the life of the truck, at http://www.arb.ca.gov/research/diesel/emissions.pdf
63) In Lien-Te Hsieh et al. above, comparing Total PCBs (in picograms) in Table 3 with Total PBDEs (in nanograms) in Table 4.
64) Quintana et al., Universidade da Coruna (Spain): Levels of POPs in airborne PM10 and PM2.5: Preliminary results, Organohalogen Compounds, Vol. 68 (2006), pp. 2507-2510, Fig. 3 (be sure to notice that PBDEs are shown in picograms (pg) and PCBs are shown in femtograms (fg); at http://www.dioxin20xx.org/pdfs/2006/06-620.pdf. or also at http://www.researchgate.net/publication/265403178_Levels_of_POPs_in_airbone_PM10_and_PM2.5_preliminary_results.
66) Halsall et al., PCBs and PAHs in UK urban air, Chemosphere, 1993, Issue 12 Vol. 26, at http://www.research.lancs.ac.uk/portal/en/publications/-(fc4aa159-f728-41af-9839-23eb55dd38ec).html
67) DellaValle et al., Environmental determinants of polychlorinated biphenyl concentrations in residential carpet dust, Environ Sci Technol. 2013 Sep 17; 47(18): 10405–10414. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076890
68) Windham et al., Autism spectrum disorders in relation to distribution of hazardous air pollutants in the San Francisco bay area. Environ Health Perspect. 2006;114(9):1438–44. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1570060/
69) Volk et al., 2011. Residential proximity to freeways and autism in the CHARGE study. Environ Health Perspect 119:873–877.
70) Roberts et al., Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ Health Study II Participants, Children's Health Volume 121 | Issue 8 | August 2013, Environ Health Perspect; DOI:10.1289/ehp.1206187 at http://ehp.niehs.nih.gov/1206187/#r35
71) Volk et al., Traffic Related Air Pollution, Particulate Matter, and Autism, JAMA Psychiatry. Jan 2013; 70(1): 71–77. 10.1001/jamapsychiatry.2013.266, NIHM SID: NIHMS578933, PMCID: PMC4019010 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019010
72) EPA web page, “Health Effects of PCBs”, at http://www.epa.gov/epawaste/hazard/tsd/pcbs/pubs/effects.htm
75) Pastor et al., Diagnosed attention deficit hyperactivity disorder and learning disability: United States 2004-2006, National Center for Health Statistics, 2008, at http://www.cdc.gov/nchs/data/series/sr_10/Sr10_237.pdf
75a) Re: PBDEs ingested by breastfed infants:
-Table 5-4 of EPA (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404, Schechter (2006) study in first page of table.(daily dose of 306 ng/kg-d for breastfed infants) Also Section 5.6.2, near end of section, of above.
- Costa et al., Developmental Neurotoxicity Of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Neurotoxicology. 2007 November; 28(6): 1047–1067. PMCID: PMC2118052 NIHMSID:
- U.S. ATSDR document on mercury at www.atsdr.cdc.gov/toxprofiles/tp46-c5.pdf, p. 443
- Code of Federal Regulations, Title 21, Chapter 1, Subchapter B, Part 165, Subpart B, Sec. 165-110 at http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfCFR/CFRSearch.cfm?fr=165.110
75c) Re: PCBs in human milk: U.S. Agency for Toxic Substances and Disease Registry, Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000, at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf This ATSDR report quotes a range of concentrations of PCBs in human milk as from 238 to 271 ng/g lipid weight. 1 g lipid weight = about 25g whole weight (assuming 4% fat in human milk). So the concentrations found in the studies were about 250 ng/25g whole weight, which = 10ng/g whole weight. 1 g (gram) = 1 ml of water., so the 10 ng/g whole weight is the same as 10ng/ml. That is the same as 10,000 ng per liter, which is the same as .01 mg/liter. So the levels of PCBs in human milk seem to be about .01 mg/liter, compared with .0005 mg/liter, the maximum allowed by law in U.S. public water systems. That is, about 20 times the concentration that would be allowed in public water systems. (U.S.EPA, Drinking Water Contaminants, National Primary Drinking Water Regulations, at http://water.epa.gov/drink/contaminants/index.cfm#Organic)
75d) Re: PBDEs in formula less than 2% of concentration in breast milk:
-Section 4.7 , 2nd paragraph (citing Schechter et al.) of U.S. EPA (2010) An exposure assessment of polybrominated diphenyl ethers. http:/cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404
-Section 5.6.2 of above, 2nd paragraph. The EPA states the figure as "44.1 ng/g lwt" (44.1 ng = 44,100 pg). For comparison purposes, the lipid (fat) weight indicated here needs to be converted to whole weight, which can be done as follows: The EPA here assumes a fat content of 4%. Using that figure, 44,100 pg/g lwt becomes 1760 pg/g wwt.
Re: Mercury in formula less than 1% as high as in human milk:
- Food Additives & Contaminants: Part B: Surveillance Volume 5, Issue 1, 2012 Robert W. Dabeka et al., Survey of total mercury in infant formulae and oral electrolytes sold in Canada DOI: 10.1080/19393210.2012.658087 at www.tandfonline.com/doi/full/10.1080/19393210.2012.658087#tabModule
-Re: PCBs in infant formula typically less than 1% but up to about 4% as high as in human milk:
- In breast milk: About 250 ng/g lipid weight. In soy-based formula: about 10 ng/g lipid weight. U.S. Agency for Toxic Substances and Disease Registry, Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000, pp. 560, 573, at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf Data does not appear to be available for PCBs in cow’s-milk-based infant formula, but data for whole milk could give an approximation, as follows: adding together the figures for the two kinds of PCBs in this study provides a range of 52 to 2455 ng/kg fat, which equals .05 to 2.45 ng/g fat (lipid) (Krokos et al., Levels of selected ortho and non-ortho polychlorinated biphenyls in UK retail milk, Chemosphere. 1996 Feb;32(4):667-73. at www.ncbi.nlm.nih.gov/pubmed/8867147)
75e) Inquiries by letters from Donald Meulenberg, Director of Pollution Action of Fredericksburg, VA, sent to the entire science team of the organization, Autism Speaks, in 2014. Meulenberg can be reached at email@example.com.
77) Breastfeeding, Family Physicians Supporting (Position Paper) -- AAFP Policies -- in American Academy of Family Physicians web site.
78) Grandjean and Jensen, Breastfeeding and the Weanling’s Dilemma Am J Public Health. 2004 July; 94(7): 1075. PMCID: PMC1448391 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1448391/
79) Autism rates associated with nutrition and the WIC program. Shamberger R.J., Phd, FACN, King James Medical Laboratory, Cleveland, OH, J Am Coll Nutr. 2011 Oct;30(5):348-53. Abstract at www.ncbi.nlm.nih.gov/pubmed/22081621
80) For details, see Appendix 2a at http://www.pollutionaction.org/breastfeeding-and-autism-and-cancer.htm
81) 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
82) Winneke, Developmental aspects of environmental neurotoxicology: lessons from lead and polychlorinated biphenyls, J Neurol Sci. 2011 Sep 15; Epub 2011 Jun 15. at http://www.ncbi.nlm.nih.gov/pubmed/21679971
83) Gascon M et al., Effects of pre and postnatal exposure to low levels of polybromodiphenyl ethers on neurodevelopment and thyroid hormone levels at 4 years of age. [Environ Int. 2011] . at www.ncbi.nlm.nih.gov/pubmed/21237513
84) Near end of Section 5.6.2 ("Impacts to Infants from Consumption of Breast Milk"), p. 5-79, of An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. online at http://www.epa.gov/ncea or directly at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404
-- The above is compatible with authoritative reports of breast milk concentrations of PBDEs (a persistent developmental toxin) being over 30 times those in infant formula: Schecter et al., Polybrominated Diphenyl Ether (PBDE) Levels in an Expanded Market Basket Survey of U.S. Food and Estimated PBDE Dietary Intake by Age and Sex, Environ Health Perspect. Oct 2006; 114(10): 1515–1520 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1626425 and also
-- PBDEs in infant formula: Section 4.7 , p. 4-77, 2nd paragraph (citing Schechter et al.) of U.S. EPA (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment; EPA/600/R-08/086F. online at www.epa.gov/ncea or directly at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404
85) 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, www.ncbi.nlm.nih.gov/pubmed/20628441. Also see footnotes 6, 15, 16, and 29 in D. Austin, An epidemiological analysis of the ‘autism as mercury poisoning’ hypothesis’, International Journal of Risk and Safety in Medicine, 20 (2008) 135-142 at http://researchbank.swinburne.edu.au/vital/access/manager/Repository/swin:9302
86) P. Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants, Environ. Health Perspectives, accepted Oct. 1993 www.ncbi.nlm.nih.gov/pmc/articles/PMC1567218/pdf Also Marques RC, et al., Hair mercury in breast-fed infants exposed to thimerosal-preserved vaccines. Eur J Pediatr. 2007 Sep;166(9):935-41. Epub 2007 Jan 20 at http://www.ncbi.nlm.nih.gov/pubmed/17237965 (Re: especially rapid mercury transmission in early postnatal weeks): Exploration Of Perinatal Pharmacokinetic Issues Contract No. 68-C-99-238, Task Order No. 13 Prepared for EPA by: Versar, Inc. EPA/630/R-01/004 Section 220.127.116.11, at http://www.epa.gov/raf/publications/pdfs/PPKFINAL.PDF
87) Volk et al., Traffic Related Air Pollution, Particulate Matter, and Autism, JAMA Psychiatry. Jan 2013; 70(1): 71–77. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019010
88) Kalkbrenner et al, Particulate Matter Exposure, Prenatal and Postnatal Windows of Susceptibility, and Autism Spectrum Disorders, Epidemiology • Volume 26, Number 1, January 2015
89) The breastfeeding rate at 12 months in 2000 (the year with data available that is most relevant to these studies) was over twice as high in California as in North Carolina. at www.cdc.gov/breastfeeding/data/NIS_data/2000/state.htm Also, in California, the breastfeeding rate at 12 months is fully 40% higher than the national average; .see CDC breastfeeding data at http://www.cdc.gov/breastfeeding/data/NIS_data/2007/state_any.htm
89a) Kalkbrenner made more reference to the third trimester as a period of high odds in comparison with earlier trimesters of gestation, but their Table 4 and Figure 2 clearly show the times of greatest odds to be after the births of most infants -- see Section 6
90) Re: postnatal vulnerability of developing brain to toxins:
PGrandjean & PJLandrigan, Developmental neurotoxicity of industrial chemicals, The Lancet, Nov. 8, 2006, at http://www.reach-compliance.eu/english/documents/studies/neurotoxity/PGrandjean-PjLandrigan.pdf : “The human brain continues to develop postnatally, and the period of heightened vulnerability (to toxins) therefore extends over many months, through infancy and into early childhood.”
Rice and Barrone:<<<<<<<<<<
EPA: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD); CASRN 1746-01-6, Section 1.a.2, at http://www.epa.gov/iris/subst/1024.htm
Also See www.autism-research.net/postnatal-effects.htm for citations of agency documents and of many peer-reviewed studies.
92) Schantz et al., Effects of PCB Exposure on Neuropsychological Function in Children, Environmental Health Perspectives • VOLUME 111 | NUMBER 3 | March 2003,
93) Kawashiro et al., Perinatal exposure to brominated flame retardants and polychlorinated biphenyls in Japan, Endocr J. 2008 Dec;55(6):1071-84. Epub 2008 Aug 22, at http://www.ncbi.nlm.nih.gov/pubmed/18719292
94) Jensen, A.A. et al, Chemical Contaminants in Human Milk, CRC Press, Inc., Boca Raton, Ann Arbor, Boston, 1991, pp. 13, 15.
96) Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. Lancet. 2006;368:2167–2178. at http://www.reach-compliance.eu/english/documents/studies/neurotoxity/PGrandjean-PjLandrigan.pdf p. 2. “Persistent lipophilic substances, including specific pesticides and halogenated industrial compounds, such as PCBs, accumulate in maternal adipose tissue and are passed on to the infant via breast milk, resulting in infant exposure that exceeds the mother’s own exposure by 100-fold on the basis of bodyweight.”
97) Statement near end of study in Quaak et al., The Dynamics of Autism Spectrum Disorders: How Neurotoxic Compounds and Neurotransmitters Interact, Int J Environ Res Public Health. Aug 2013; 10(8): 3384–3408, Published online Aug 6, 2013. doi: 10.3390/ijerph10083384 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3774444/
98) Vodicnik MJ, Lech JJ. The transfer of 2,4,5,2’,4’,5’-hexachlorobiphenyl to fetuses and nursing offspring. Toxicol Appl Pharmacol 1980;54:293-
99) Kodama et al., Transfer of Polychlorinated Biphenyls to Infants from their Mothers, Archives of Environmental Health: An International Journal, Vol. 35, 1980 at http://www.tandfonline.com/doi/abs/10.1080/00039896.1980.10667472#.VNS9NC5mpME.
100) U.S. EPA: The Effects of Great Lakes Contaminants on Human Health, at http://www.epa.gov/greatlakes/health/report.htm
101) Bose-O’Reilly et al., Mercury Exposure and Children’s Health, Curr Probl Pediatr Adolesc Health Care. Curr Probl Pediatr Adolesc Health Care. 2010 Sep; 40(8): 186–215, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3096006/
102) Needham et al., Partition of Environmental Chemicals between Maternal and Fetal Blood and Tissues, Environ Sci Technol. Feb 1, 2011; 45(3): 1121–1126. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031182 “Cord serum concentrations of lipophilic substances … averaged only 20% of those occurring in maternal serum….while milk levels tend to be about 50% higher than the maternal serum.”
-- Concise International Chemical Assessment Document 55. Polychlorinated biphenyls: human health aspects. Geneva: WHO, 2003.
103) Thompson et al., Thyroid Hormone Action in Neural Development, Cereb. Cortex (2000) 10 (10): 939-945. doi: 10.1093/cercor/10.10.939 at http://cercor.oxfordjournals.org/content/10/10/939.long
106) Zoeller et al., Timing of Thyroid Hormone Action in the Developing Brain: Clinical Observations and Experimental Findings, Journal of Neuroendocrinology, Vol. 6, Issue 10, pages 809–818, October 2004 at http://www.bio.umass.edu/biology/zoeller/pdf/JNeuroendo.pdf
107) Derksen-Lubsen et al., Neuropsychologic development in early treated congenital hypothyroidism: analysis of literature data, Pediatr Res. 1996 Mar;39(3):561-6. at www.ncbi.nlm.nih.gov/pubmed/8929881
111) EPA-452/R-97-009 December 1997, pp. 5-29 (Section 5.6.1) at http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf; this EPA report to Congress stated, “neuronal migration, a process specifically affected by methylmercury …continues until five months after birth.”
-- Tau et al., Normal Development of Brain Circuits, Neuropsychopharmacology. Jan 2010; 35(1): 147–168. Published online Sep 30, 2009. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055433 “cortical neurogenesis and neuronal migration continue through the postnatal period (Bhardwaj et al, 2006; Shankle et al, 1999”
-- Stiles et al.,The Basics of Brain Development, Neuropsychol Rev. Dec 2010; 20(4): 327–348. Published online Nov 3, 2010 at http://www.ncbi.nlm.nih.gov/pmc/articles/pmc298900; “The mature organization of the neocortex emerges over a protracted time during the postnatal period”
-- Kostovic et al., Developmental Reorganization of the Human Association Cortex during Perinatal and Postnatal Life, Neurodevelopment, Aging and Cognition 1992, pp 3-17 at
http://link.springer.com/chapter/10.1007%2F978-1-4684-6805-2_1#page-1 “The reorganizational events in the human cerebral cortex extend at least up to the third year of postnatal life….”
-- Watson et al., Postnatal growth and morphological development of the brain: a species comparison, available at http://www.deepdyve.com/lp/wiley/postnatal-growth-and-morphological-development-of-the-brain-a-species-2ypG86N0aQ/12 October, 2006. “During (postnatal) synaptogenesis, neurons migrate….” “Prefrontal cortex synaptogenesis occurs…to about 15 months of age.”
-- Kostovic, Structural and histochemical reorganization of the human prefrontal cortex during perinatal and postnatal life. Prog Brain Res. 1990;85:223-39, at http://www.ncbi.nlm.nih.gov/pubmed/2094895
-- Myoshi et al., GABAergic Interneuron Lineages Selectively Sort into Specific Cortical Layers during Early Postnatal Development Cereb Cortex. Apr 2011; 21(4): 845–852. Published online Aug 23, 2010 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059886/ “…suggesting that the final laminar location of interneurons is determined during the postnatal period …cortical interneurons continue to migrate during early postnatal stages,”
--- Hatten et al., Central nervous system neuronal migration, Annu Rev Neurosci. 1999;22:511-39. at http://www.ncbi.nlm.nih.gov/pubmed/10202547?dopt=Abstract&holding=npg “…. In the postnatal period, a wave of secondary neurogenesis produces huge numbers of interneurons ….”
-- JM Fuster, MD. PhD, The Prefrontal Cortex, Fourth Edition, Elsevier, 2009 at http://www.sciencedirect.com/science/book/9780123736444 “…whereas the basic cytoarchitecture in the human prefrontal cortex is pre-established at birth, its fine development continues for many years…. This fact may have momentous implications for cognitive development….” (p. 15) Note that the brain defects observed in the Stoner et al study were as follows: in patches about ¼” long, surrounded by normal tissue, “mild abnormalities” were detected, specifically “decreases” in certain types of cells and in expression of certain types of genes. Those deviations sound more closely related to “fine development” (which occurs postnatally) than the basic cytoararchitecture, which is established prenatally.
-- Shankle et al., Approximate doubling of numbers of neurons in postnatal human cerebral cortex and in 35 specific cytoarchitectural areas from birth to 72 months. Pediatr Dev Pathol. 1999 May-Jun;2(3):244-59. at http://www.ncbi.nlm.nih.gov/pubmed/10191348 (The title, if read carefully, conveys the essential message.)
112) Stoner et al., Patches of Disorganization in the Neocortex of Children with Autism, n engl j med 370;13 nejm.org march 27, 2014, at http://www.nejm.org/doi/full/10.1056/NEJMoa1307491at http://www.nejm.org/doi/full/10.1056/NEJMoa1307491
115) Osius et al., Exposure to Polychlorinated Biphenyls and Levels of Thyroid Hormones in Children, Environmental Health Perspectives, Volume 107, Number 10, October 1999, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566609/pdf/envhper00515-0109.pdf
116) (Huisman et al., Perinatal exposure to polychlorinated biphenyls and dioxins and its effect on neonatal neurological development, Elsevier, Early Human Development, 41 (1995)111-127, at http://www.sciencedirect.com/science/article/pii/037837829401611R)
117) American Nurses Association, "The Imperative of Breastfeeding," 2010, at http://www.nursingworld.org/MainMenuCategories/Policy-Advocacy/Positions-and-Resolutions/Issue-Briefs/Breastfeeding.pdf
118) Weber et al., Female employees' perceptions of organisational support for breastfeeding at work: findings from an Australian health service workplace, International Breastfeeding Journal 2011, 6:19 doi:10.1186/1746-4358-6-19 at http://www.internationalbreastfeedingjournal.com/content/6/1/19
119) Dachew et al., Breastfeeding practice and associated factors among female nurses and midwives at North Gondar Zone, Northwest Ethiopia: a cross-sectional institution based study, International Breastfeeding Journal 2014, 9:11 doi:10.1186/1746-4358-9-11, at http://www.internationalbreastfeedingjournal.com/content/9/1/11
3g) Lorber et al., Infant Exposure to Dioxin-like Compounds in Breast Milk, Environmental Health Perspectives, June, 2002, Vol. 110, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240886/pdf/ehp0110-a00325.pdf
3k) U.S. ATSDR: Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000 at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf, pp. 21, 18 The ATSDR refers to “extensively corroborated findings in experimental animals that exposure to PCBs in utero and/or during early development (e.g., through breast milk) can deplete levels of circulating thyroid hormones in the fetus or neonate, which may give rise to a hypothyroid state during development. The Danish Health and Medicines Authority says essentially the same thing except that they indicate greater certainty about the expected result of low thyroid. (Danish Health and Medicines Authority, 2013, Health risks of PCB in the indoor climate in Denmark, at http://sundhedsstyrelsen.dk/publ/Publ2013/12dec/HAofPCBindoorDK_en.pdf)
3l) Developmental Neurotoxicity of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Costa et al., Neurotoxicology. 2007 November; 28(6): 1047–1067. doi: 10.1016/j.neuro.2007.08.007 PMCID: PMC2118052 NIHMSID: NIHMS34875 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052/
3u) NIH web page at http://www.nlm.nih.gov/medlineplus/ency/article/001193.htm
3v1) EPA web pages on Particulate Matter and Particulate Matter 2.5 at http://www.epa.gov/cgi-bin/broker?_service=data&_debug=0&_program=dataprog.national_1.sas&polchoice=PM
3w) Chen et al., Thyroid hormones in relation to lead, mercury, and cadmium exposure in the National Health and Nutrition Examination Survey, 2007-2008, Environ Health Perspect. 2013 Feb;121(2):181-6. doi: 10.1289/ehp.1205239. Epub 2012 Nov 15. at http://www.ncbi.nlm.nih.gov/pubmed/23164649 This study of 4400 adults found an inverse association between mercury exposure and thyroid hormones.
3w0) EPA web page at http://www2.epa.gov/international-cooperation/persistent-organic-pollutants-global-issue-global-response; see PCBs entry in The “Dirty Dozen” chart
3w1) EPA, Office of Solid Waste and Emergency Response, EPA530-R-05-006. Sept. 2005, Human Health Risk Assessment Protocol for Hazardous Waste Combustion Facilities, Section 2.3.9, p. 111; (best accessible by doing a Google search for “EPA, Office of Solid Waste and Emergency Response, EPA530-R-05-006,” and clicking on the result that shows the above document number).
3x2) Section 4.1 of ATDSR document on PBDEs at http://www.atsdr.cdc.gov/toxprofiles/tp68-c4.pdf
3x2a) U.S. ATSDR, Nov. 2000: Toxicological Profile for Polychlorinated Biphenyls (PCBs) at http://www.atsdr.cdc.gov/ToxProfiles/tp17.pdf, p. 480:
3x4) WHO Working Group, Polychlorinated biphenyls and terphenyls (Second edition) , Environmental Health Criteria Vol:140 (1993) 682, found on the U.S. National Library of Medicine’s http://toxnet.nlm.nih.gov, using their search tool >
(3x5) NIH, U.S. National Library of Medicine, Toxtown, Particulate Matter, at http://toxtown.nlm.nih.gov/text_version/descriptions.php?id=21&type=2
3x5a) EPA web page on particulate matter at http://www.epa.gov/pm
3x5b) EPA web page on PM-2.5 (PM2.5 Mobile Breakdown) at http://www.epa.gov/cgi-bin/broker?_service=data&_program=dataprog.national_2.sas&_debug=0§or=Mobile&polchoice=PM25_PRI
3x5c1) U.K. Air Quality Expert Group, Fine Particulate Matter (PM2.5) in the United Kingdom, 2012, at http://uk-air.defra.gov.uk/assets/documents/reports/cat11/1212141150_AQEG_Fine_Particulate_Matter_in_the_UK.pdf pp. 82, 85
(3x5g) World Bank Group, Pollution Prevention and Abatement Handbook, Airborne Particulate Matter, 1998, p. 202, at http://www.ifc.org/wps/wcm/connect/59cfb38048855493b35cf36a6515bb18/HandbookAirborneParticularMatter.pdf?MOD=AJPERES
(3x6) .Bitema et al., Polychlorinated biphenyls in ambient air of NW Greece and in particulate emissions, Environment International, Volume 31, Issue 5, July 2005, Pages 671–677 at http://www.sciencedirect.com/science/article/pii/S0160412004002089
(3x8) Wikstrom et al., Secondary formation of PCDDs, PCDFs, PCBs, PCBzs, PCPhs and PAHs during MSW combustion, Organohalogen Compounds, Vol. 36(1998), at http://www.dioxin20xx.org/pdfs/1998/98-508.pdf, p. 66
(a) Sonawane, U.S. EPA, Chemical Contaminants in Human Milk: An Overview, Environmental Health Perspectives, 1995, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1518901/pdf/envhper00365-0192.pdf
00d) EPA web pages on Persistent, Bioaccumulative and Toxic (PBT) Chemical Program, at http://www.epa.gov/pbt/pubs/background.htm and http://www.epa.gov/pbt/pubs/aboutpbt.htm. PCBs and mercury were among the first 12 such substances that were identified; PBDEs, which are chemical relatives of PCBs and dramatically increasing in human bodies in very recent decades, were not identified until later.
(0.1b) re PBDEs: EPA: Emerging Contaminants: Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyls (PBB) , 2008, at http://nepis.epa.gov/Adobe/PDF/P1000L3S.PDF.
Also: EPA, Building a Database of Developmental Neurotoxicants: Evidence from Human and Animal Studies at http://epa.gov/ncct/toxcast/files/summit/48P%20Mundy%20TDAS.pdf
Mercury and PCBs have long been known to be neurodevelopmental toxins.
(0a1) Milbrath et al., Apparent Half-Lives of Dioxins, Furans, and Polychlorinated Biphenyls as a Function of Age, Body Fat, Smoking Status, and Breast-Feeding,Environ Health Perspect. 2009 Mar; 117(3): 417–425. Published online 2008 Oct 3. doi: 10.1289/ehp.11781, at http://ehp.niehs.nih.gov/11781/
(0d1) Eckenhausen et al., Organochlorine Pesticide Concentrations in Perinatal Samples from Mothers and Babies, Archives of Environmental Health: An International Journal, Vol. 36, Issue 2, 1981, at http://www.tandfonline.com/doi/abs/10.1080/00039896.1981.10667611#.VOEi7S5mpME
(0e1) Lorber et al., Infant Exposure to Dioxin-like Compounds in Breast Milk, Environmental Health Perspectives, Volume 110 | Number 6 | June 2002, Table 4, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240886/pdf/ehp0110-a00325.pdf
-- Knoll et al.,, Intake, fecal excretion, and body burden of polychlorinated dibenzo-p-dioxins and dibenzofurans in breast-fed and formula-fed infants, at http://www.ncbi.nlm.nih.gov/pubmed/8910931 This study was cited in a 2002 EPA document ("Infant Exposure to Dioxin-like Compounds in Breast Milk") that apparently considered it to be fully valid.
(0e9) 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 18.104.22.168, at www.epa.gov/raf/publications/pdfs/PPKFINAL.PDF
(0e10) For a thorough presentation on this topic, including citations of many peer-reviewed and authoritative sources, see www.autism-research.net/postnatal-effects.htm.
(0.f) Karmaus et al., Early Childhood Determinants of Organochlorine Concentrations in School-Aged Children, Pediatric Research (2001) 50, 331–336; doi:10.1203/00006450-200109000-00007
old(1) Mercury Emissions from Motor Vehicles, at http://www.epa.gov/ttnchie1/conference/ei13/toxics/hoyer.pdf
Hsieh et al., Reduction of Toxic Pollutants Emitted from Heavy-duty Diesel Vehicles by Deploying Diesel Particulate Filters, Aerosol and Air Quality Research, 11: 709–715, 2011 ISSN: 1680-8584 print / 2071-1409 online doi: 10.4209/aaqr.2011.05.0058 at http://aaqr.org/VOL11_No6_November2011/8_AAQR-11-05-OA-0058_709-715.pdf
old(2) EPA: "... the average daily dose to the infant over (a year of breastfeeding) is predicted to be about 60 pg of TEQ/kg-d." (U.S. EPA. Estimating Exposure To Dioxin-Like Compounds - Volume I: Executive Summary, EPA/600/8-88/005Ca., 2002, revised 2005, at http://cfpub.epa.gov/si/si_public_record_Report.cfm?dirEntryID=43870, in Section II.6, "Highly Exposed Populations", 4/94 (p. 39)
The above 60 pg compares with the EPA's "RfD" (estimated relatively safe dose) for dioxin of 7 × 10−10 mg/kg-day." (that is, O.7 pg of TEQ/kg-d) (see EPA’s 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD); CASRN 1746-01-6 at http://www.epa.gov/iris/subst/1024.htm) The EPA has estimated the average adult background exposure to be 1-3 pg TEQ/kg of body weight/day.
In another EPA-provided document: Infant Exposure to Dioxin-like Compounds in Breast Milk, Lorber and Phillips Vol. 110. No. 6, June 2002 • Environmental Health Perspectives, at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download , referring to a breastfed infant’s initial “estimated body weight-based exposure of 242 pg TEQ/kg-day. After one year of breast-feeding, the exposure drops to about 18 pg TEQ/kg-day.”
Also Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. Lancet. 2006;368:2167–2178. at http://www.reach-compliance.eu/english/documents/studies/neurotoxity/PGrandjean-PjLandrigan.pdf p. 2.
old5) Mocarelli et al., Perinatal Exposure to Low Doses of Dioxin Can Permanently Impair Human Semen Quality, Environ Health Perspect. May 2011; 119(5): 713–718. Published online Jan 24, 2011. doi: 10.1289/ehp.1002134 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3094426/
See several mercinhalatn files!
mercStatesCA file re merc (v. high in CA) that is shorter-term in body, which (along with long avg. duration of bfing) could explain why CA study showed effects of current exposures, cf. nationwide study that shows mainly effects of long-term accumulations.
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