Studies of Links between Autism and Environmental Exposures, including Infant Feeding
Section 1: Evidence of neurodevelopmental effects of pesticides and related chemicals
Section 1.a: Authoritative study finding very strong association between autism and developmental exposure to pesticides, in a dose-effect relationship
Section 1.b: A subsequent study and other information indicating major postnatal vulnerability to effects of pesticides:
a) Greater vulnerability after birth, found in this study
b) Authoritative recognition of postnatal vulnerability of the developing brain to toxins, including pesticides
c) Greatly increased exposure postnatally
Section 1.c: Strong evidence of major placental reduction of fetal exposure to such chemicals
Section 1.d: Additional evidence of pesticide exposures’ typically being dramatically increased postnatally
Section 2: Multiple pollutants in a normal infant food that could be related to neurodevelopmental disorders
Section 2.a: Four pollutants mainly in developed countries, plus DDT mainly in the developing world
Section 2.b: The major pathway of DDT to infants
Section 3: Studies indicating that prevalence of autism is related to toxins in human milk
Section 3.a: Epidemiological studies, including evidence of a dose-response relationship
Section 3.b: Major laboratory study providing disturbing biological evidence about link between autism and exposure to widespread environmental toxins
Section 3.c: Studies indicating association between traits of ASD and infants’ exposures to the rapidly-increasing PBDEs.
Section 3.d: Other studies indicating adverse neurological effects of PCBs and dioxins
Section 3.e: Postnatal developmental effects of mercury, and evidence of inappropriate reluctance to acknowledge postnatal vulnerability to neurological toxins
Section 4: Evidence indicating that exposures to pesticides (both newer and older) continue to be sources of neurodevelopmental harm
Section 4.a: Organochlorine pesticide exposure continues to be serious.
Section 4.b: The newer pesticides are also harmful.
Section 4.c: A study finding substantial developmental effects of urban background exposures to one of the newer pesticides
Appendix A: Substantial exposure of Americans to ingestions of organochlorine pesticides via food imports, especially in seafood
Appendix B: Biological details about harm to the brain caused by newer pesticides
Appendix C: The AAFP’s ignoring of research of the last two decades
Appendix D: Specifically postnatal vulnerability of the developing brain to pesticide exposure
Section 1: Evidence of neurodevelopmental effects of pesticides
Section 1.a: Authoritative study finding very strong association between autism and developmental exposure to pesticides, in a dose-effect relationship
The study described below (Roberts et al.) was published in 2007 by a team of researchers who are authors (first or contributing) of a total of 923 published studies. The study found six times the normal risk of ASD among children whose mothers at time of birth lived near pesticide application areas in California. According to that study, ASD risk increased with the poundage of pesticides applied “and decreased with distance from field sites.”1 The study analyzed data regarding 465 children with ASDs along with 15 control subjects per case. Most of the pesticide applied in the area was dicofol or endosulfan, both of which have been used on cotton, fruits, vegetables, beans, and nuts, and are organochlorine pesticides.
The pesticide exposures of mothers and developing fetuses/infants who lived closest to the pesticide application areas were clearly high in comparison to general population exposures, but effects of exposures at more widespread background levels are apparent in the following:
-- Increased ASD risk was also found in this study farther away from the fields and where amounts applied were reduced. So intermediate exposures to the pesticides were also associated with increased ASD, just not as far in excess of the normal prevalence of ASD.
-- In another study in California, the authors found that exposures of urban populations to pesticides were similar to those of agricultural populations, and they attributed the urban exposure mainly to pesticides in foods.2
a) Greater vulnerability after birth, found in this study:
After completing a thorough statistical analysis of the above study’s data and state records of pesticide applications, an affiliated study found that, in addition to a prenatal period of vulnerability to pesticide exposures, there was an even stronger vulnerability during the first year after birth. The likelihood that the finding of postnatal vulnerability would have been a result of chance alone was .003, or 3 out of 1000; that was a four-times-lower likelihood of chance occurrence than applied to the finding of a prenatal period of vulnerability (.013).3
b) Authoritative recognition of postnatal vulnerability of the developing brain to toxins: The above finding of postnatal vulnerability to pesticides’ effects may seem surprising, considering the widespread belief that vulnerability of developing organs to harm by toxins is basically during gestation. But it should not be surprising at all, to someone who is familiar with research published in the last two decades. A commission of the U.S. National Research Council (of the National Academies), in a document entitled, “Pesticides in the Diets of Infants and Children,” refers to “specific periods in development when toxicity can permanently alter the function of a system;” such periods of special vulnerability to toxins are said to apply to development of the central nervous system (the brain and spinal cord), which the commission says “may demonstrate particular sensitivity (to toxins) during the postnatal period.”4
There is considerable other evidence refuting the notion that only the prenatal period is a time of substantial vulnerability to developmental toxins in the environment, including the following which is summarized from www.disability-origins.info:
(1) (from Section 3 at the above link): over 30 published studies that have found developmental harm to be associated with infants’ and children’s postnatal exposures to common environmental toxins while finding less or no effects of prenatal exposures to those same toxins.
(2) (from Section 1 at above link): statements from many eminently authoritative sources, such as
-- “… in the early months after birth, children and fetuses are particularly sensitive to the harmful effects” of toxins.” (ATSDR)
-- The early-postnatal period (along with the prenatal period) is a time of “greatest risk” for vulnerability to developmental toxins.(NIH)
-- “The periods of embryonic, foetal and infant development are remarkably susceptible to environmental hazards.” (An international group of 24 experts)
-- “Neurotoxic effects of a number of environmental agents have been demonstrated in various studies, with critical windows of vulnerability to these agents occurring both pre- and postnatally.” (EPA researchers)
Details about all of the above, as well as much more evidence about postnatal vulnerability to widespread environmental toxins, with authoritative sources cited for all of the evidence, can be found at www.disability-origins.info.
According to a European/American team of scientists, many pesticides used in agriculture “target the nervous system of insect pests,” which is of special concern because of the “similarity in brain biochemistry” between insects and humans.5
This topic will be continued in Appendix D, citing many studies that have observed postnatal vulnerability to neurological effects of pesticides, including
-- doubled incidence of pervasive development disorder (the classification of which autism/ASD is a part) linked with a common increase in children’s exposure to a widespread pesticide, and
-- 2.4 times the incidence of ADHD among children with detectable versus non-detectable levels of another widely-used pesticide. See Appendix D.
c) Greatly increased exposure postnatally: Providing additional verification of the nature of fetal-versus-postnatal exposure as indicated above, a 2010 study by an American-Danish-German team of nine researchers (Needham et al.) measured cord serum levels and breast milk levels of 87 environmental chemicals, including pesticides. Among organohalogen compounds (which include DDT and other organochlorine pesticides), umbilical cord serum had one-fifth the average concentration of those chemicals compared with maternal serum, when figured on a volume basis; by contrast, breast milk had 285% higher average concentrations of the chemicals than the maternal serum;6 this resulted in a total average breast milk concentration 19 times that of the cord serum, There was found to be considerable variation among the various chemicals studied, but the overall average milk-to-cord-serum concentration ratio for the 87 chemicals studied was 19 to 1.
Also of relevance: according to various authors describing California farmworkers being studied, nearly all of the mothers breastfeed their infants, for an average duration of 6 months;7 therefore, when reading about the apparent neurodevelopmental effects of pesticides on children in California agricultural communities such as in the Roberts et al. study above, one would reasonably suspect that the major pathway by which those pesticides were ingested by the developing infants (who would be disproportionately impaired) was via nursing; and that notion would be strongly reinforced by the Bradman et al. study in Section 1.d.
For much more about the greatly increased exposure of infants to pesticides postnatally, see Section 1.d.
Section 1.c: Additional evidence of placental reduction of fetal exposure to such chemicals:
The standard term “placental barrier” has considerable relevance, although an alternative phrase “filter with variable effectiveness” would be more accurately descriptive. A study’s finding was presented in the previous section about 80% placental reduction of fetal exposure to pesticides compared with maternal serum. In addition,
-- A 1996 study in India reported that “the average level of DDT in breast milk, maternal serum and cord serum were found to be 1.27, 0.27 and 0.14 ngL-1, respectively.”8 So DDT in umbilical cord serum was half as high as in maternal serum (and only 11% as high as in breast milk). Other studies have found compatible differences in that same direction.9
-- An American study, by a team of researchers who are authors (first or contributing) of a total of 163 published studies among them (Eyster et al.), arrived at findings relevant to the above concerning other organohalogen chemicals and their presence in human fluids. (Organohalogens include DDT, other organochlorine pesticides, and PBBs.) Umbilical cord blood was found to contain “one-tenth of the concentration found in maternal serum….” (referring to PBBs) (By contrast, “Human milk contained PBBs at 107 to 119 times the quantity found in maternal serum.”)10 According to the U.S. ATSDR, PBBs have been used as flame retardants in “a variety of consumer products, such as computer monitors, televisions, textiles, and plastic foams” (as found in most cushioning). The ATSDR also points out that PBBs are “able to leave the plastic and find their way into the environment.”11 Although discontinued in the U.S., their use has apparently continued in some imported products;12 and, as of a 2009 American study, PBBs “remain a public health concern because of their environmental persistence.”13
Quoting again from the above ATSDR publication, “Changes in nerve and brain function have been seen in animals that were exposed to PBBs in the womb and by nursing.” Bear in mind that PBBs have been found to be ingested by nursing infants in concentrations over a thousand times the prenatal exposure (see the Eyster et al. study cited above).
The persistent and lipophilic (attracted to fats) nature of organohalogens is what explains their accumulation to high concentrations in breast tissue, before they are mobilized during lactation. At the prenatal stage, the placental barrier is what leads to the reduced concentrations in umbilical cord serum, and therefore reduced exposure of the fetus. The early postnatal period is well recognized to be a period of continued vulnerability to developmental effects of toxins, with dozens of studies having found that postnatal exposures have greater effects than prenatal exposures to specific toxins (Section 1.b, item b). More evidence about increased exposures of infants to pesticides via breastfeeding will be presented below.
Section 1.d: Additional evidence of exposures to pesticides typically being dramatically increased via lactation:
To sum up the preceding: Autism was found, in an authoritative study, to be six times as likely among children whose mothers at time of birth were living near fields where organochlorine pesticides were applied. (Section 1.a) The most pronounced period of effects of those toxins was found to have been during the year after birth (Section 1.b, item a), which is a period recognized to be one of strong vulnerability to effects of developmental toxins. (Section 1.b, item b) Almost all children in such California agricultural areas are breastfed, for an average of about 6 months, and breast milk has been found to have 19 times higher concentrations of the chemical group that includes DDT and other organochlorine pesticides, compared with umbilical cord serum (Section 1.b, item c); this is partly because of the concentrating effect that occurs when toxins accumulate in fat tissues and are later mobilized via lactation, and partly because of the effects of the placental barrier. (Section 1.c)
To help complete the picture, it needs to be pointed out regarding increased exposures of infants to pesticides via breastfeeding, in addition to what was presented in Section 1.b item c and Section 1.c above, there is also evidence from other studies about greatly varying concentrations of pesticides or their metabolites in infants and children in correlation with their feeding histories. Those included the following:
-- concentrations of DDT and some PCBs ten times as high in breastfed infants as in bottle-fed infants after six months of breastfeeding, as found in a 2005 study in Germany;14
--- organochlorine concentrations found to be already almost six times as high in breastfed infants as in bottle-fed infants after only six weeks of breastfeeding;15
--- organochlorine concentrations (including metabolites of DDT) still four times as high in breastfed infants as in bottle-fed infants at age four, and still two and a half times as high at age 14, as found in a 2015 study in a western country (Spain) in which DDT (the chief organochlorine) was banned in 1977.16
In line with the known concentrating effect of lactation, it is of interest to read a statement of two leading experts on toxins involved in child development (P Grandjean and PJ Landrigan, first or contributing authors of 326 and 47 scientific studies, respectively); they concluded that “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.”17
In a 2006 study in which breast milk samples from Denmark and Finland were examined, 13 different pesticides were detected in each of at least 90% of the 130 breast milk samples tested, in addition to other pesticides found less frequently. The average concentrations were over 10 times the lowest concentrations measured, and there was no indication that the lowest levels measured were especially low.18 A 2011 study (Weldon et al.), investigating pesticides in breast milk samples from the urban Bay Area and a rural area in California, found detection rates almost identical to the above; the authors noted that their findings for urban populations were not far below those for agricultural populations, and attributed the urban exposure mainly to pesticides in foods.19
The above should be compared with detections of pesticides in infant formula, as reported by authoritative sources:
a) Quoting from a publication of a commission of the U.S. National Academy of Sciences, “measurements have consistently demonstrated that no pesticides are detected in finished infant formulas. These invariably negative analytical findings are attributable to ingredient selection and processing procedures that reduce the potential for pesticide residues to appear in the finished product.”20
b) In 2013, the U.S. Department of Agriculture reported testing over 300 samples of infant formula and finding no detectable pesticide in 100% of dairy-based formula tested and in 99.4% of soy-based formula. That essentially clean slate for infant formula was not because of insensitivity of the testing; only 35% of fruit and vegetable samples tested were found to be free of pesticides.21
The reader should make careful note of the above, to better appreciate the difference in the toxicities of contents of two main alternative infant feeding types. To summarize the above: In two separate studies, over a dozen different pesticides or pesticide-related chemicals were found in each of at least 90% of breast milk samples. By contrast, in a publication of the National Academy of Sciences as well as in a thoroughly-studied report of the U.S. Department of Agriculture, only one sample of infant formula out of several hundred tested was found to contain as much as one pesticide.
So it seems safe to say that there are night-and-day differences in the exposures that developing infants receive to pesticides, depending on their feeding type. Therefore it is important to consider evidence of effects of pesticides on development of children. One authoritative study finding a very strong association of pesticide exposure with autism, in a dose-response relationship, was described in Section 1.a; and that connection was found to be especially close with regard to exposures that took place during the year after birth. (Section 1.b) Additional correlations of DDT with neurological deficits 10 and 15 years after time-of-birth exposures are presented in the next section (see Figure 2 and text above and below it). The above studies dealt with exposure to organochlorine pesticides, which have been mostly phased out in developed countries; but they are still widely used in developing countries, with exposures typically far exceeding established safe levels, and exposures to them are still significant even in developed countries due to food imports, especially of seafood. (to be described in Section 4.a) The newer pesticides that have largely replaced the organochlorines in developed countries have been found in the overwhelming majority of studies to also be neurologically harmful, including in relation to prevalence of ASD, but also in association with general loss of IQ. (see Section 4.b, later)
It should be expected that, in agricultural areas, infants’ exposures to pesticides could be substantial via pathways other than breast milk. But, according to the only readily-found study dealing with this topic (Bradman et al., measuring urine samples in about 400 children in a California rural community), breastfeeding is likely to be the predominant source of exposure for the vast majority of infants at six months of age, even in such communities.22
If infant formula is not available or affordable, or is no longer called for, cow’s milk is likely to be a viable alternative for avoiding the pesticides in human milk. The only readily-found study comparing pesticides in cow’s milk with those in human milk found organochlorine insecticides (especially DDT derivatives) to be 20 times lower in cow’s milk than in human milk.23 Crops grown for cattle feed are not sprayed with pesticides significantly, since cattle feed is not expected to be free of insect damage; and toxins don't have a chance to accumulate in cows, since the toxins are continuously cleared out by milking.
Section 2: Multiple pollutants in human milk that are probably linked to neurodevelopmental disorders:
Although human milk contains various components that are beneficial, there is considerable evidence about various components of typical breast milk (in addition to pesticides) that are harmful to neurological development. Some of that evidence will be presented here, to provide background that will help the reader understand the meaning of the studies that will come next.
Section 2.a Four pollutants mainly in developed countries, plus DDT mainly in the developing world
During the last half century or so, toxins that have become widespread in the environment have also become substantial contaminants in human milk.24 Contemporary breast milk includes five toxins, most of which are neuro-developmental toxins,25 at levels greatly exceeding governmentally-established thresholds for safety. The first four are at high levels mainly in developed countries, and the last one (DDT) is high mainly in developing countries.
(a) dioxins, exceeding the EPA’s Reference Dose (estimated reasonably safe dose, or RfD) by scores to hundreds of times;26
(b) PBDEs, normally well above and up to 20 times the EPA’s RfD;27
(c) mercury, typically four times the maximum allowed by U.S. law in bottled water, but in many cases much higher than that,28 and
(d) PCBs, in human milk in concentrations about 20 times the maximum allowed by law in U.S. public water supplies.29
(e) DDT, exceeding WHO/FAO’s acceptable daily intake (ADI) in various developing countries according to at least four separate studies, and exceeding it by as much as 100 times in Asian countries.30
Four of the above toxins (and possibly all five) are present in infant formula in concentrations less than 10% as high, and usually less than 1% as high, as their concentrations in human milk.31
All of the above information is accurately based on statements from authoritative sources, which are referred to in the footnotes.
DDT is not (yet) recognized as a neurodevelopmental toxin, but
(a) it is an organochlorine pesticide, which is the general kind that was used in the fields near which ASD rates were six times as high as normal, as found in the Roberts et al. study (Section 1.a), and
(b) there are other excellent reasons to believe that DDT is a neurodevelopmental toxin, as will be seen below.
Exposures at about time of birth to DDT have been found to have strong correlations with neurological deficits in the children ten and fifteen years later. As seen in the upper chart below (from ref.32), starting with average DDT levels in mothers at time of birth in various geographic areas (10 countries and 14 German states), higher average time-of-birth DDT levels correlated well with lower average mental capacities in children in those same locations 15 years later.
Also, as seen just above, average DDT levels at about time of birth in the 14 German states correlated well with percentages of “backward” children in those states 10 years later. (Backward was defined as children “visiting special schools because of decreased learning capability.”)
Section 2.b: The major pathway of DDT to infants:
DDT levels in the above study were measured in breast milk, although much of the apparent neurodevelopmental harm associated with those maternal DDT levels may possibly have resulted from prenatal exposures. But remember that postnatal exposures are many times greater than prenatal exposures, during a period when the brain’s development continues to be vulnerable to effects of environmental toxins:
-- as indicated earlier, concentrations of DDT were found to be ten times as high in breastfed infants as in bottle-fed infants after six months of breastfeeding, in a 2005 study in Germany, decades after banning of DDT;14
-- the average level of DDT in breast milk was found to be nine times that in cord serum in a 1996 study in India;33
--- organochlorine concentrations (including metabolites of DDT) were found to be still four times as high in breastfed infants as in bottle-fed infants even at age four, as found in a 2015 study in Spain, where DDT had been banned decades earlier.16
-- remember also from Section 1.d that, in the only readily-found study comparing pesticides in cow’s milk with those in human milk (Adamović et al.), organochlorine insecticides (especially DDT derivatives) were found to be 20 times as high in human milk as in cow’s milk.34
-- In a Dutch study, it was estimated that about half of a fully-grown mother’s intake of DDT was excreted to the small infant by lactation, whereas there was so little DDT in fetal blood that it could not even be studied.35
that (a) a human mother’s burden of DDT accumulates over many years before it
is excreted to nursing infants,36 and (b) a cow’s
intake of DDT is continuously excreted as part of high-volume, daily milking
and therefore has little chance to accumulate, it should not be surprising that
and its derivatives were found to be 20 times as high in human milk as in cow’s
milk. The above is in addition to the statements in publications of
both the U.S. National Academy of Sciences and the U.S. Department of
Agriculture indicating that no pesticides were found in any of hundreds
of samples of cow’s-milk-based infant formula that were tested. (see Section 1.d)
For considerable information verifying the postnatal vulnerability of the developing brain to environmental toxins, including (a) statements from many authoritative sources and (b) referral to dozens of studies that found greater adverse effects of postnatal exposures to toxins compared with prenatal exposures to the same toxins, see Section 1.b.b.
Given all of the above, there appears to be ample reason to believe that the apparent harm done to developing brains by the elevated maternal levels of DDT (see Fig. 2) probably resulted much more from postnatal exposures to DDT than from prenatal exposures. The finding that organochlorine concentrations (including metabolites of DDT) were still four times as high in breastfed infants as in bottle-fed infants even at age four,16 combined with compatible findings in other studies, indicates that it was probably breastfeeding that was the main determinant of the differences in amounts of DDT to which the developing infants were exposed.
It is well known, but unexplained, that over four times as many male children as female children are diagnosed with ASD. This chart shows levels of DDE (a metabolite of DDT) in serum of U.S. males and females, decades after banning of DDT in the U.S.; it shows that male children absorb and retain many times more DDT than female children, while their neurological development is taking place. Considering the evidence of neurodevelopmental harm caused by DDT, could DDT’s disproportionate absorption by males help explain the male-female differences in autism prevalence?
If the reader feels that the answer to the above question is “yes,” the next step is to consider the principal means by which infants are exposed to DDT. (see the first part of Section 2.b)
Based on information presented above, the question just below has been presented to a number of scientists, at least some of whom should be in a position to answer it:
Are there any toxins known to widely reach infants in doses exceeding a recognized safe level, aside from the several such toxins that are ingested by means of breast milk? If so, please identify them.
This question was mailed to seven members of the science team at the major autism-advocacy organization, Autism Speaks; as of several months later, of the three responses received, not one offered an answer to that question. And not one reply questioned the validity of the statement about toxicity of normal contents of breast milk.
After over a year of the above question’s being asked very publicly (in web pages that receive considerable traffic), nobody seems to be able to provide an answer to it. That should be considered to be very significant. If any reader can offer an answer to the above question, or can suggest somebody who might be able to offer an answer, please respond to firstname.lastname@example.org
Section 3: Studies indicating that prevalence of autism is related to toxins in human milk:
Section 3.a: Epidemiological studies, including apparent dose-response relationships:
-- Autism prevalence was found in a study by a highly-published scientist to correlate with breastfeeding rates and duration, drawing on data for all 50 U.S. states and 51 U.S. counties. This included findings that "exclusive breast-feeding shows a direct epidemiological relationship to autism" and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism." (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 )
-- Another U.S. study found that 37% of children with autism had been breastfed for at least 6 months, as compared with 13% in the comparison group and 14% of infants in the state. The P value was .003, indicating three chances in a thousand that this relationship could have been a random occurrence. (Breastfeeding and Autism P. G. Williams, MD, Pediatrics, University of Louisville, and L. L. Sears, MD, presented at International Meeting for Autism Research, May 22, 2010, Philadelphia Marriot, found at https://imfar.confex.com/imfar/2010/webprogram/Paper6362.html)
-- A U.K. study of 1189 children with ASD found an unusually high percentage of ASD cases had been exclusively breastfed for more than four weeks: 65%. (Whitely et al., Trends in Developmental, Behavioral and Somatic Factors by Diagnostic Sub-group in Pervasive Developmental Disorders: A Follow-up Analysis, Autism Insights: 2009:1 3–17 pp. 10, 14 at http://www.la-press.com/redirect_file.php?fileId=2425&filename=1725-AUI-Trends-in-Developmental,-Behavioral-and-Somatic-Factors-by-Diagnostic-.pdf&fileType=pdf. A comparison figure for equivalent general U.K. breastfeeding (exclusive at four weeks) is 28%, as found in the U.K. Infant Feeding Survey - UK, 2010 Publication date: November 20, 2012, Chapter 2, at http://www.hscic.gov.uk/catalogue/PUB08694/ifs-uk-2010-chap2-inc-prev-dur.pdf An almost identical figure was found in the next-earlier U.K. Infant Feeding Survey (2005).
-- A 2010 Canadian study, drawing data from a population-based “clinically-rich perinatal database,” investigated a very large population, nearly 130,000 births. Data from almost 127,000 of those children (those without identified genetic risk of autism) went into the study’s finding that there was a 25% increased risk of autism among children who were breastfed at discharge from the hospital. Dodds et al., The Role of Prenatal, Obstetric and Neonatal Factors in the Development of Autism, J Autism Dev Disord (2011) 41:891–902 DOI 10.1007/s10803-010-1114-8, Table 6, at http://autism.medicine.dal.ca/research/documents/2011DoddsetalJAutDevDisord.pdf
Note that all of the above studies appear to support a conclusion that, the greater the exposure to breast milk, the greater the level of autism among the breastfed infants. In the Dodds study, using discharge from the hospital as the dividing line for breastfeeding exposure, there was a 25% higher autism rate among the breastfed children. In the Whitely study, the duration of breastfeeding used for the comparison was four weeks, which was associated with a 130% (65/28) higher-than-normal level of autism. In the Williams study, the duration of breastfeeding used for comparison was a full six months, which was associated with an approximately 175% (37/13.5) higher rate of autism. That same kind of correlation was also found in the Shamberger study: "direct correlation (of increased autism rates) with the increasing percentage of women exclusively breast-feeding" and also with the "longer duration" of breastfeeding.
Section 3.b: Major laboratory study providing disturbing biological evidence about link between autism and exposure to widespread environmental toxins
As published in Proceedings of the National Academy of Sciences, biological evidence of a possible link between toxins in breast milk and autism was provided in a 2007 animal study carried out in the laboratory of and written by M.M. Merzenich, a member of the U.S. National Academy of Sciences.<Kenet et al., Perinatal exposure to a noncoplanar polychlorinated biphenyl alters tonotopy, receptive fields, and plasticity in rat primary auditory cortex, 2007, The National Academy of Sciences of the USA, 7646–7651 _ PNAS _ May 1, 2007 _ vol. 104 _ no. 18 www.pnas.org_cgi_doi_10.1073_pnas.0701944104 at http://www.pnas.org/content/104/18/7646.full.pdf > According to Dr. Merzenich, “PCB intoxication was achieved by feeding the rat mother just enough of the poison to match the levels of PCB recorded in nursing human mothers in high-PCB-exposure areas of the U.S.”<Merzenich, What underlies the documented increase in autism incidence? Results of a new study, from On the Brain, by Dr. Michael Merzenich, 26 April 2007, at http://www.onthebrain.com/2007/04/underlies-documented-increase-autism-incidence-results-new-study> The study noted that the specific form of PCB that they tested is one of the types that “predominate in breast milk samples.” Dr. Merzenich pointed out that, although exposure of the fetal rats began early in pregnancy, “after birth, the mother delivered it to the infants in even-more-concentrated levels — because PCBs are concentrated 5- or 6X in breast milk.” The study pointed out that “there is as much as a 6.6-fold increase of plasma PCB concentrations in (human) infants who were breastfed for more than 3 months relative to infants who were not breastfed.”
The effects found in the above study were that the baby rats had “grossly distorted development of the primary auditory cortex” of the brain. According to Dr. Merzenich, “normal, progressive development (of the infant rats’ brains) was almost completely blocked,” about half of the rats had a “dramatically altered organization of the representations of sound frequency,” and this was “of special interest because the same bizarre abnormalcies have been recorded in autistic individuals.”Burton, Hearing: PCBs Alter Brain Development, Environ Health Perspect. 2007 Aug; 115(8): A400. PMCID: PMC1940069 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940069/>
Going into more detail, maps of the auditory sections of the brains of the PCB-exposed rats were found to be oddly shaped and had holes in them, many neurons showed a lack of normal function, and the typical distribution of neurons was disorganized. T. Kenet, the first author of the study and later a faculty member at Harvard Medical School, said “This must affect how their brains interpret sound.”<Burton, Hearing: PCBs Alter Brain Development, Environ Health Perspect. 2007 Aug; 115(8): A400. PMCID: PMC1940069 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940069/> The scientists also recorded imbalances in the affected brains that would affect representation of sound, which the authors said was consistent with evidence of such imbalance “as a core abnormality of autism.” According to a summary of the study in a web page of Harvard University, “the key mechanism that the brain uses for learning new skills in all animal species and humans” was found to be impaired. <National Scientific Council on the Developing Child, Science Briefs: Prenatal and Infant Exposure to an Environmental Pollutant Damages Brain Architecture and Plasticity (2007). Retrieved 6/28/2015 from www.developingchild.net.
The doses received by the nursed rat pups were at levels equivalent to the high end of recorded U.S. background exposure, and those doses “resulted in a grossly distorted development” of the brain’s primary auditory cortex, according to the authors. If doses equivalent to high human background exposures have such severe effects on rats, there would appear to be good reason to also be concerned about more typical human exposures.
The study’s authors also noted that reports of declines of some forms of PCBs in the environment do not necessarily apply to this “more stable and prevalent” type of PCB.<Kenet et al. 2007>
Dr. Merzenich pointed out that, in addition to PCBs, we should also be concerned about PBDEs, which are “close cousins” of PCBs, and which have been “approximately doubling in concentration in American bodies every 2-5 years;” PBDEs, like PCBs, accumulate especially in fat and breast milk. He concluded, “If human fetal and infant effects parallel rat impacts, we would predict that there would be a correlation between the PCB/PBDE levels in human breast milk — and in infant blood — with the probability of autism onset.” And there is reason to think that effects on human infants would have a good chance of being similar to effects on rats; animal testing is a standard way of predicting likely effects of toxins on humans -- not perfect, but good, and it is the best means of testing toxicity to humans that is available.<WHO, Persistent Organic Pollutants: Impact on Child Health, p. 6
The study’s authors stated that, since the rat pups in the study did not have a genetic susceptibility to a developmental disorder, the vulnerability of human infants to the toxins might be greater in genetically susceptible human populations than it was in the rats. <Class of PCBs causes developmental abnormalities in rat pups, UCSF News Center, Univ. of California San Francisco, by Jennifer O’Brien, April 23, 2007, at http://www.ucsf.edu/news/2007/04/5564/class-pcbs-causes-developmental-abnormalities-rat-pupsat >
One of the study’s authors (I.N. Pessah, Professor of Molecular Biosciences, University of California at Davis and Director of the UC Davis Center for Children’s Environmental Health), when referring to other environmental toxins that are related to PCBs (such as PBDEs) to which infants are also exposed, stated that “the current finding could be just the tip of the iceberg.”(ibid.UCSF news)
Section 3.c: Studies indicating associations between traits of ASD and infants’ exposures to the rapidly-increasing PBDEs.
Given the reasonable concerns (expressed just above) about toxic effects of PBDEs, their rapid increases in the environment in recent decades, and the many-times higher levels of PBDEs in human milk than in infant formula (see Section 1.b of www.breastfeeding-toxins.info), it is relevant to see what was found in some more recent studies of effects of that chemical, including in leading to traits that are basic or frequent characteristics of ASD:
-- A 2011 study found that gestational exposure to PBDEs in the mothers in a study had no significant adverse effect, but exposure to those same mothers' PBDE levels via breastfeeding did have a substantial effect, including an 80% increase in relative risk of attention-deficit problems and a 160% increased relative risk of poor social competence. Gascon M. et al., Effects of pre and postnatal exposure to low levels of polybromodiphenyl ethers on neurodevelopment and thyroid hormone levels at 4 years of age. Environ Int. 2011 Apr;37(3):605-11. doi: 10.1016/j.envint.2010.12.005. Epub 2011 Jan 14 found at www.ncbi.nlm.nih.gov/pubmed/21237513 (Note that poor social competence is a basic trait of autism, and attention deficits are a frequent characteristic of those with ASD.)
-- A 2012 study of 290 breastfed Spanish children found that those who consumed breast milk containing a form of PBDEs commonly found in contemporary breast milk (BDE 209) for a breastfeeding period of 16 weeks or less had average negative mental test (BSID) scores of -1.07, and those exposed to it for a breastfeeding period of more than 16 weeks had average negative scores over three times as great (-3.48).Gascon et al., Polybrominated Diphenyl Ethers (PBDEs) in Breast Milk and Neuropsychological Development in Infants, in Environ Health Perspect. 2012 December; PMCID:PMC3548276 At http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3548276. Bear in mind that (a) this showed apparent effects of PBDEs present in the milk of a group of relatively typical European mothers; and (b) American breast milk has been found to be 10 to 100 times higher in PBDEs than the levels found in Europe. (EPA: An Exposure Assessment of Polybrominated Diphenyl Ethers. Washington, DC, USA: USEPA; 2010.)
-- A 2010 review article looked at thyroid effects of PBDEs (thyroid supply is known to be crucial to development of the brain), as well a long-term effects of PBDEs, and found support for a hypothesis of PBDEs as autism risk factors. Polybrominated diphenyl either (PBDE) flame retardants as potential autism risk factors Anne Messer, 2010 Elsevier Physiology and Behavior 100 (2010) 245-249 at http://www.ncbi.nlm.nih.gov/pubmed/20100501.
Section 3.d: Another study indicating ASD-related effects of PCBs:
A 2014 study (Jusko et al., by a team of 16 researchers) found close correlation between reduced hearing ability and increased PCB levels linked with breastfeeding. (See chart below about child PCB levels in relation to duration of breastfeeding.). Bear in mind that hearing deficits (and the resulting impaired learning ability and reduced speech development) are common among those with ASD. A 2016 study (Bennetto et al.37) found children with ASD to have a specific hearing impairment, with severity of autism varying in relation to the degree of hearing impairment. Also remember from the Kenet/Merzenich study the serious damage to the auditory sections of brains of nursed infant rats that apparently resulted from PCB concentrations equivalent to some human background exposures. (Jusko et al., Prenatal and Postnatal Serum PCB Concentrations and Cochlear Function in Children at 45 Months of Age, Environmental Health Perspectives • volume 122 | number 11 | November 2014, at http://dash.harvard.edu/bitstream/handle/1/13454664/4216161.pdf?sequence=1
Notice in this chart from the Jusko et al. study the dramatic differences in children’s PCB levels at 45-months of age, according to duration of breastfeeding. Then remember the demonstrated serious destructive effects of PCBs on development of rats’ brains. (Section 3.b)
According to the EPA's web page on health effects of PCBs, "Effects of PCBs on nervous system development have been studied in monkeys and a variety of other animal species. Newborn monkeys exposed to PCBs showed persistent and significant deficits in neurological development, including visual recognition, short-term memory and learning. Some of these studies were conducted using the types of PCBs most commonly found in human breast milk." EPA web page on health effects of PCBs at http://www.epa.gov/osw/hazard/tsd/pcbs/pubs/effects.htm
According to an article in an industrial health journal, "Even low levels of dioxin or PCB exposure during the perinatal period can greatly influence neurological development" in this way and "can cause irreversible neurological damage." Industrial Health 2000, 38, 259–268 Review Article: The Effects of Dioxin on Reproduction and Development Junzo YONEMOTO National Institute for Environmental Studies, Japan p. 262; at http://www.jicosh.gr.jp/en/indu_hel/pdf/IH38_33.pdf
Also Glorieux et al., 1988; Rovet et al., 1987; Haddow et al., 1999)." (Prioritization of Toxic Air Contaminants -- Children's Environmental Health Protection Act (State of California), October, 2001
Of interest is a study that its authors described as the only one that has been carried out on the association between background exposure to persistent organic pollutants (such as dioxins, PCBs and PBDEs) and clinically significant developmental disorders, such as learning disability or attention deficit disorder, among children from a general human population. It utilized data for 278 children aged 12–15 who were included in the U.S. National Health and Nutrition Examination Survey 1999–2000. The authors found dramatically increased odds of the children’s having these disorders if they had detectable levels of dioxins The average odds ratio of having Learning Disability for those with detectable levels of dioxins, compared with those without detectable levels, was 2.33 (that is, a 133% increased likelihood); and the average odds ratio of having Attention Deficit Disorder for those with detectable levels of dioxins/furans, compared with those without detectable levels, was 3.02 (three times as likely). Lee et al., Association of serum concentrations of persistent organic pollutants with the prevalence of learning disability and attention deficit disorder, J Epidemiol Community Health 2007;61:591–596. doi: 10.1136/jech.2006.054700 at http://jech.bmj.com/content/61/7/591.full.pdf+html. Note that these effects were found not in a group of children with exceptionally high exposures, but in a group comprised of the (approximately) 30% of the population with the highest dioxin concentrations. This study should be seen in combination with findings by a two-researcher team headed by an EPA senior scientist (citing five other studies with compatible findings) indicating that accumulated exposure to dioxins was expected to still be twice as high among the breastfed children even after 10 years. Lorber et al., Infant Exposure to Dioxin-like Compounds in Breast Milk, Volume 110 | Number 6 | June 2002 • Environmental Health Perspectives (a peer-reviewed journal published by the National Institute of Environmental Health Sciences of NIH) http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download Also, in a 2011 study, by 13 scientists, it was determined that at ages18 to 26, average dioxin concentrations were still twice as high in the breastfed young men as in those who had been formula fed. 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. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3094426/ It would be reasonable to assume from the above that by far the principal determinant of the extent of a developing child’s dioxin exposure and accumulation is breastfeeding. And, as indicated by the study that was apparently the only one to assess effects of dioxin exposure on neurological development of older children in the general population (see above), increased dioxin exposure (at levels such as typically found in human milk) apparently can have serious effects. It is especially noteworthy that this study dealt with children old enough to give a reasonable indication of long-term effects of the toxins, as opposed to essentially all of the other studies assessing effects of such toxins, which tested children at much younger ages, before long-term effects would be likely to be well demonstrated.
In another study of effects of toxins in breast milk on children at a more valid age for assessing the lifetime effects, formula-fed children at age 9 performed better than their breastfed counterparts; and the children who were breastfed for longer periods performed worse than those breastfed for shorter periods, in scores on a test of executive function. Vreugdenhil et al., Effects of Perinatal Exposure to PCBs on Neuropsychological Functions in the Rotterdam Cohort at 9 Years of Age, Neuropsychology, 2004, Vol. 18, No. 1, 185–193 at http://psycnet.apa.org/journals/neu/18/1/185.pdf
In this prospective study (therefore allowing accurate measures of exposures, compared with retrospective studies) the authors grouped the children into six different categories, according to shorter or longer durations of breastfeeding, formula feeding, and higher or lower exposures of each of those groups to perinatal toxins. The formula-fed children performed better than their breastfed counterparts, and the children who were breastfed for longer periods performed worse than those breastfed for shorter periods, in scores on a test of executive function. Those relationships held consistently, when the subjects were grouped according to both higher prenatal exposures to toxins and lower prenatal exposures to toxins. Scores of formula-fed children were only insignificantly higher than those of children breastfed for shorter durations (6 to 16 weeks)
Section 3.e: Postnatal developmental effects of mercury:
The pesticides that had been applied in the area investigated in the Roberts et al. study (Section 1.a) were organochlorines, which have been mostly phased out in the U.S. and other developed countries; this may give the impression that people in developed countries no longer need to be concerned about exposures to and effects of those pesticides, but that would be a false impression. Organochlorine pesticide exposure continues to be serious, and the newer pesticides are also harmful, as will be explained in detail below.
Section 4.a: Organochlorine pesticide exposure continues to be serious all over the world
Organochlorine pesticides are still widely used in developing countries, with the results that
(1) people in developed countries also, especially in the U.S., are exposed to DDT via substantial food imports (see below), and
(2) many millions of infants in the developing world are exposed to the organochlorine pesticide, DDT, in concentrations far exceeding authoritatively-established safe guidelines. First notice (in the chart below) that DDT levels to which infants are commonly exposed in Tunisia -- shown on the bottom line -- were about in the middle of exposures in the various countries with data shown.
Since exposure of breastfed infants to DDT in Tunisia appears to be about in the middle of the widely-ranging exposure levels in the world, it is worth considering the significance of this medium level of exposure of developing infants (via a source of exposure that is very normal in that country (Exclusive breastfeeding rates in Tunisia were reported to be about 47%, as of a 2008 report UNICEF report) World Breastfeeding Week 2008, MENA Regional Fact Sheet, at www.unicef.org/media/images/fact_sheet.doc “Exclusive breastfeeding in MENA (Middle East and North Africa) is highest in Tunisia (47%, 2000)”, below Graph 4. , with over 90% breastfeeding at initiation (Bouanene et al., at http://www.ncbi.nlm.nih.gov/pubmed/21473131, and La Leche League statistics at http://www.lalecheleague.org/cbi/bfstats03.html)).
Notice in this chart (from same source as the larger chart above) that the average estimated daily intake (EDI) of infants in a country with mid-level infant exposure to DDT is 20% higher than the tolerable daily intake (TDI) set by Health Canada, which is also the acceptable daily intake set by FAO/WHO (Okonkwo et al., http://www.ncbi.nlm.nih.gov/pubmed/18663399)) Then consider how much the tolerable/acceptable guidelines would be exceeded in the many countries where exposures are much higher than in Tunisia; just looking at the averages shown in the larger chart (not to mention above-average exposures), the safe guidelines would be far exceeded by millions of infants.
To complete the picture,
a) the reader should notice that, as seen in the text of the larger chart above, “human breast milk” is a known pathway to the infant of these chemicals in concentrations that far exceed established safe levels;
b) also notice, in the smaller chart, that the average estimated daily intakes in Tunisia for PCBs and HCHs, also, are at or close to the ADIs; then observe in the larger chart that the average breast milk concentrations of those chemicals in other countries typically far exceed the (near-hazardous) levels in Tunisia;
c) since the question remains as to whether there could be other major pathways (other than breastfeeding) by which an infant could take in the pesticides in hazardous concentrations, remember that breastfeeding was found to be the predominant source of pesticides in infant urine at 6 months even in an agricultural community with direct pesticide exposure. 22
Remember also (from Section 1.b. part c, Section 1.c, and Section 1.d) the extreme differences between infant exposures to organochlorines via human milk compared with fetal exposure or exposures via infant formula: 19 times as high in breast milk as in umbilical cord serum (as found in the Faroe Islands), 9 times as high in breast milk as in umbilical cord serum (as found in India), 10 times as high in breastfed infants as in bottle-fed infants at six months (as found in Germany), four times as high in breastfed children as in bottle-fed children at age 4 (as found in Spain), and more.
Keep in mind that, in addition to the high exposures of millions of infants to DDT in developing countries, exposures to pesticides in general (including the newer ones) are also still a matter of serious concern in the U.S., and probably other developed countries as well. As mentioned, the organochlorines (older types of pesticides) are still very much a part of typical U.S. diets by way of their presence in food imports. According to a web page of the U.S. National Oceanographic and Atmospheric Administration, 91% of seafood consumed in the U.S. is imported, about half of that is farmed, and a very large part of it comes from Asia,.U.S. NOAA, Fishwatch: U.S. Seafood Facts, The Surprising Sources of Your Favorite Seafoods, at http://www.fishwatch.gov/features/top10seafoods_and_sources_10_10_12.html where most seafood accumulates substantial concentrations of organochlorines in its contents. This is indicated by the chart in Appendix A, in which the key words are “daily intakes of typical persistent organic pollutants (pesticides) via consumption of aquatic products,” shown by continent. Notice that the continent (Asia) from which a large part of American seafood comes is an extreme standout in pesticide concentrations, and American seafood products also stand out from most of the world in pesticide concentrations. Also, over $19 billion worth of food (mostly fruits and vegetables) is imported to the U.S. each year from a country where levels of DDT are very high -- Mexico (see second chart near beginning of Section 4.a). A more complete presentation on this topic needs to be rather long and has therefore been placed in Appendix A.
Section 4.b: The newer pesticides are also harmful.
The research findings about the 13 different pesticides present in 90% of breast milk samples (in Section 1.d) were from recent years and therefore applied largely to the newer pesticides. The findings in that same section about absence of pesticides in infant formula were from both the period of the older pesticides and the period of mainly newer pesticides.
The organochlorines have been largely replaced in developed countries with newer pesticides that were originally presumed to be safer (organophosphates, pyrethroids, carbamates, etc.), but those have turned out to be similarly harmful. According to Dr. David Bellinger, professor at the Harvard School of Public Health and author (contributing or primary) of over 250 published studies, the total loss of IQ points associated with exposure to organophosphate pesticides alone is over twice as great as the total losses associated with ASD, and almost 60 times as great as the losses associated with the well-known neurological toxin, methylmercury.Bellinger, A Strategy for Comparing the Contributions of Environmental Chemicals and Other Risk Factors to Neurodevelopment of Children, Environ Health Perspect. 2012 Apr; 120(4): 501–507. PMCID: PMC3339460 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3339460/ This strongly implies that there is substantial loss of intelligence in the general population (including in developed countries) that results from some of the newer pesticides, well beyond the links with autism implied by the Roberts et al. study described in Section 1.a.
The persistence of the organochlorines in the environment and in humans was thought to be largely responsible for their recognized harmfulness. But since the effectiveness of the pesticides that have been replacing the organochlorines is of much shorter duration, those chemicals need to be applied more often to maintain the intended protection from pests. Considerable evidence has been found in recent years indicating that the newer pesticides, in addition to typically being neurologically harmful (see Bellinger statement above), have also been found to be present in human breast milk. Non-persistent Pesticides Found in U.S. Mothers' Breast Milk, Bridges, Spring 2012, Regents of the University of California, Center for Occupational and Environmental Health, at http://coeh.berkeley.edu/bridges/Spring2012/PesticidesBM.html, referring to the findings of the study, Weldon et al., A pilot study of pesticides and PCBs in the breast milk of women residing in urban and agricultural communities of California, Journal of Environmental Monitoring, DOI: 10.1039/c1em10469a, at http://ehsdiv.sph.berkeley.edu/holland/publications/files/Weldon2011.pd Quoting from a statement by the first author of a 2012 study (Weldon et al.), referring to the newer pesticides, “it was thought previously that they wouldn’t be found in breast milk,… how exposure to non-persistent pesticides affects most people is still largely unknown.” Non-persistent Pesticides Found in U.S. Mothers' Breast Milk, Bridges, Spring 2012, Regents of the University of California, Center for Occupational and Environmental Health, at http://coeh.berkeley.edu/bridges/Spring2012/PesticidesBM.html
Non-awareness of health effects of the newer pesticides, as indicated in the statement just above (from 2012), is no longer an accurate description of the state of the knowledge on this subject. Ample evidence has been accumulated to the effect that the newer pesticides are neurodevelopmentally harmful, of which the above statement by Dr. Bellinger is only the beginning. In a book entitled, “Pesticides in the Diets of Infants and Children,” a commission of the U.S. National Research Council (of the National Academies) states, “Certain classes of pesticides, including organophosphates, carbamates, and organochlorines, are known to have neurotoxic effects….” <<Pesticides in the Diets of Infants and Children, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C. 1993, p. 25 at http://www.nap.edu/openbook.php?record_id=2126&page=109 A 2013 review article reported on the results of many earlier studies, stating that “exposure to organophosphate pesticides is associated with poorer neurodevelopment of children.” The authors then went on to specify various neurological deficits that have been found to be associated with organophosphate pesticides, in nine different scientific studies (which they cited). They pointed out that “Only one current cross-sectional study… did not find an association between exposure to pesticides and the neurodevelopment of children ”.(Jurewicz et al., Chemical exposure early in life and the neurodevelopment of children – an overview of current epidemiological evidence, Annals of Agricultural and Environmental Medicine 2013, Vol 20, No 3, 465–486, at http://www.ncbi.nlm.nih.gov/pubmed/24069851 A separate (2013) review article reported that “27 studies evaluated showed some negative effects of pesticides on neurobehavioral development. A positive dose-response relationship between OP (organophosphate pesticide) exposure and neurodevelopmental outcomes was found in all but one of the 12 studies that assessed dose-response.” (A dose-response relationship is considered to be especially good evidence of a causal relationship.)(Munoz-Quezada and ten others, Neurodevelopmental effects in children associated with exposure to organophosphate pesticides: a systematic review, Neurotoxicology, 2013 Dec;39:158-68. at http://www.ncbi.nlm.nih.gov/pubmed/24121005 A 2008 study stated that its own findings, in addition to “a number of experimental studies (the authors then cited six such studies) have begun to document the deleterious effects of OP (organophosphate) pesticides in neurodevelopment.” (Lizardi et al., The Effects of Organophosphate Pesticide Exposure on Hispanic Children's Cognitive and Behavioral Functioning, Oxford Journals, Journal of Pediatric Psychology, (2008) Vol. 33 Issue 1, at http://jpepsy.oxfordjournals.org/content/33/1/91.long)
In a study published by the American Academy of Pediatrics, investigating some neurological effects of organophosphate pesticides, it was found that “children with levels higher than the median of detectable concentrations had twice the odds of ADHD … compared with children with undetectable levels.” (That same study found that 94% of children tested had detectable concentrations.) Bouchard et al., Attention-Deficit/Hyperactivity Disorder and Urinary Metabolites of Organophosphate Pesticides, Pediatrics, Vol. 125 No. 6 June 1, 2010, pp. e1270 -e1277 at http://pediatrics.aappublications.org/content/125/6/e1270.full So background exposure to these widely-used pesticides, in concentrations that were merely above average for the general population, were associated with twice the odds of ADHD, compared with exposures resulting in undetectable levels. (Note that ADHD overlaps with ASD) It is probable that, if measurements were taken of children with top-quarter or top tenth exposures to the pesticides, the odds of having this major neurological disorder would be far more than twice as high as in children with undetectable exposures.
When summarizing data from 37 unique studies, the authors of a 2014 review article found that 34 (92%) reported an association between estimated exposures to environmental toxicants and ASD. Most of the reviewed studies were said to have had good study designs, and “the toxicants that appeared to have the strongest association with ASD were pesticides and air pollutants.”(Rossignol et al., Environmental toxicants and autism spectrum disorders: a systematic review, Transl Psychiatry. 2014 Feb; 4(2): e360. PMCID: PMC3944636 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3944636/) Note that, although those two categories of toxic exposures were considered to be similar in how closely associated they were with ASD, pesticides were the only category that was at least moderately specific; the field of “air pollutants” encompasses an enormous range of thousands of possibly-implicated toxins, including pesticides. If the relatively narrow category of pesticides is about as implicated with harmful effects as an entire very large category of toxins, the narrower category would logically seem to be the one that should receive especially close, specific attention.
Biological details about harm to the brain caused by the newer pesticides can be found in Appendix B.
A study indicating harmfulness of one of the most widely-used newer pesticides (Rauh et al.) was carried out by a team of nine researchers, who are authors (lead or contributing) of over 2000 published scientific studies among them. (Rauh and 8 others, Impact of Prenatal Chlorpyrifos Exposure on Neurodevelopment in the First 3 Years of Life Among Inner-City Children, Pediatrics, 2006 Dec; 118(6): e1845–e1859. NIHMSID: NIHMS382766 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390915/) They investigated effects on children of chlorpyrifos, which (according to the EPA) is currently widely used in the U.S., including on corn, soybeans, fruit and nut trees, cranberries, broccoli, cauliflower, and other row crops; it has also been used for residential pest control. Notice in this chart the large differences in various neurological problems in 3-year-old children according to whether they had received higher or lower exposures to chlorpyrifos. The “high exposures” were not results of poisonings; the children were ordinary inner city children in New York City, who merely had higher exposures to the pesticide than a large percentage of their local contemporaries.
In addition to the dramatic differences shown in the above chart, “At 36 months of age, the odds of highly exposed children having mental delays were 2.4 times as great… and the odds of motor delays were 4.9 times as great….” Continuing, “…adverse cognitive and psychomotor effects increased over time.” Explaining the seriousness of the above results, the authors noted that “compromised motor performance in the preschool years is a significant precursor of subsequent educational performance deficits.” They also pointed out, citing eight studies as evidence, that “the developing brain could be vulnerable to organophosphate pesticide exposure from early embryonic life into childhood.” They measured the pesticide in umbilical cord blood and referred to the exposures as prenatal; however -- as just indicated -- they acknowledged that effects of the pesticide could result from postnatal exposures; the elevated cord blood levels that they measured (a time-of-birth measurement) would have been tenuous indications of exposures during gestation since (as the authors said) most of a dose of chlorpyrifos is eliminated from the body within a few days. So the authors were relying on an assumed stability over time of the mothers’ exposures; but that assumption would provide equal support to an expectation that the time-of-birth measurements were valid indications of most infants’ exposures after birth via nursing. As indicated above, with very substantial evidence, the developing brain is also vulnerable to toxins postnatally (Section 1.b, item b), and postnatal exposures to pesticides (via breastfeeding) are considerably greater than prenatal exposures from the same mother. (Section 1.d)
Since ADHD overlaps with ASD, it should be mentioned that a 2013 publication of WHO stated, “Attention deficit/hyperactivity disorder (ADHD) is overrepresented in populations with elevated exposure to organophosphate pesticides.” (WHO: State of the Science of Endocrine Disrupting Chemicals - 2012, accessible at http://www.who.int/ceh/publications/endocrine/en/
The fact that Rauh et al. (above) did not mention the alternative exposure route of lactation probably has a great deal to do with the prevailing groupthink position to the effect that breastfeeding is not only beneficial but that nothing significantly negative about it should be said. The source of many millions of dollars of grant money for research studies, the U.S. Department of Health and Human Services, makes clear what it does and does not want to hear from researchers, at its web page at http://womenshealth.gov/breastfeeding/OWH_FS_Breastfeeding_7-25-2014.pdf; there one reads totally positive recommendations about breastfeeding except in very unusual circumstances, with not a single mention of the word “toxin.” In the 10-page online position statement on breastfeeding of the American Academy of Pediatrics, (accessed 8/16/2015 at http://pediatrics.aappublications.org/content/early/2012/02/22/peds.2011-3552) the word “toxin” does not appear even once; it cites many studies finding benefits of breastfeeding, but there is no mention of any of the 60+ studies that have found adverse effects of breastfeeding.(see www.breastfeeding-studies.info) The breastfeeding position paper of the American Academy of Family Physicians at least acknowledges the (undeniable) presence of toxins in human milk, but it maintains the expected silence about the extensive research that has been published about adverse effects of breastfeeding; more about that is in Appendix C.
Appendix A: Substantial exposure of Americans to ingestions of organochlorine pesticides via food imports, especially in seafood:
According to a web page of the U.S. National Oceanographic and Atmospheric Administration, 91% of seafood consumed in the U.S. is imported, and about half of it is farmed..U.S. NOAA, Fishwatch: U.S. Seafood Facts, The Surprising Sources of Your Favorite Seafoods, at http://www.fishwatch.gov/features/top10seafoods_and_sources_10_10_12.html China alone produces more than two-thirds of the farmed fish in the world.Monterey Bay Aquarium, Turning the Tide, The State of Seafood, 2nd Ed. 2011, p. 15 at http://www.seafoodwatch.org/-/m/c4de19eac4f24657a23f12e17b392b2c.pdf Consumption of (mostly imported) seafood in the U.S. is an important determinant of organochlorine levels in breastfeeding mothers, for the following reasons: According to a team of scientists with the Chinese Academy of Sciences, who cited five studies in support of their 2010 statement that follows, “Numerous researchers have shown that human dietary exposure to POPs (including organochlorine pesticides) is largely attributable to consumption of aquatic products.” Yu et al., Dietary Intake of Persistent Organic Pollutants and Potential Health Risks via Consumption of Global Aquatic Products, Environmental Toxicology and Chemistry, Vol. 29, No. 10, pp. 2135–2142, 2010, SETAC, DOI: 10.1002/etc.315 at http://onlinelibrary.wiley.com/doi/10.1002/etc.315/pdf And, according to a study by a team of four Korean scientists, “fish generally contain higher levels of OCs (organochlorines) than any other food category.”(Yim et al., Levels of persistent organochlorine contaminants in fish from Korea and their potential health risk, Archives of Environmental Contamination and Toxicology, April 2005, Volume 48, Issue 3, pp 358-366 at http://link.springer.com/article/10.1007/s00244-004-0085-1 >>
The above statements of Asian scientists are probably biased by the extremely high level of organochlorines in Asian aquatic products (see chart, from the above Yu et al. study). But, especially since a very high percentage of seafood consumed in the U.S. comes from Asia, and considering that American seafood is also rather high in organochlorines (see chart), those statements about aquatic products’ being dominant sources of organochlorines to humans should be valid in relation to U.S. mothers who eat seafood.
The extreme variability of exposures to organochlorine pesticides according to specific country, especially in the case of China, is illustrated by the following: In a study published in 2009, estimated daily intake of DDT per capita in South China was found to be about 11,000 times the per capita intake in Cambodia, and over 2700 times the average intake in Indonesia. Guo et al., Organochlorine pesticides in seafood products from Southern China and health risk assessment, Environmental Toxicology and Chemistry, Table 4, Article first published online: 9 DEC 2009, DOI: 10.1897/06-446R.1, at http://onlinelibrary.wiley.com/doi/10.1897/06-446R.1/abstract?userIsAuthenticated=false&deniedAccessCustomisedMessage=
It would be reasonable to assume that a good part of that regional high level of ambient organochlorine pesticide would become part of the water supply for area aquaculture, via drainage from soil tilled in regional farming as well as by atmospheric transport.According to a publication of the Delaware Division of Public Health, “Organochlorine pesticides accumulate in the environment. They are very persistent and move long distances in surface runoff or groundwater.”Organochlorine Pesticides, Frequently Asked Questions, Delaware Health and Social Services, at http://www.dhss.delaware.gov/dph/files/organochlorpestfaq.pdf See also U.S. Dept. of Agriculture: Imports From China and Food Safety Issues, Economic Information Bulletin No. 52, pp. 5-9 at http://www.ers.usda.gov/media/156008/eib52_1_.pdf Most of the organochlorine pesticides are very persistent; the best-studied pesticide in this category, DDT, has a half-life in agricultural soils of 4 to 35 years. Wang et al., Organochlorine pesticides in soils under different land usage in the Taihu Lake region, China, Journal of Environmental Sciences 19(2007) 584–590 at http://www.jesc.ac.cn/jesc_en/ch/reader/create_pdf.aspx?file_no=2007190512
There is good evidence that DDT has especially long life in the underwater habitats of fish and other aquatic life: Organochlorine pesticides, including DDT, were banned from agricultural uses in 1983. But a 2008 study, overseen by an official of the Guangzhou Institute of Geochemistry of the Chinese Academy of Sciences, “still found high levels of DDT in surface water samples, suspended particulate matter, and sediments.”.<Royal Society of Chemistry, News, China's environment gets a health check, 20 March 2008, at http://www.rsc.org/chemistryworld/News/2008/March/20030802.asp, A 2011 study of concentrations of organochlorine pesticides (including HCH) in various kinds of Chinese soils found that “out of all of the land cover types, the paddy fields retained the highest amount of HCHs due to the soil being submerged in water.” (Yang et al., Residues of Organochlorine Pesticides (OCPs) in Agricultural Soils of Zhangzhou City, China, Pedosphere 22(2): 178–189, 2012, ISSN 1002-0160/CN 32-1315/P c_ 2012 Soil Science Society of China, Published by Elsevier B.V. and Science Press. The long lives of organochlorines in sediment and suspended particulate matter, combined with continued input via soil erosion from regional farmland, would keep levels of these pesticides at elevated levels well into the future in aquaculture water; that would also apply in shallow offshore fishing waters, such as the heavily-fished Yellow Sea off the China coast. It should not be surprising that organochlorine pesticides still show up in high concentrations in fish from Asia.
A 1997 study referred to presence of a substantial percentage of DDT (an organochlorine pesticide) in meat and fish from Southeast Asian countries. <Kannan et al., Organochlorine pesticides and polychlorinated biphenyls in foodstuffs from Asian and oceanic countries., Rev Environ Contam Toxicol. 1997;152:1-55. at http://www.ncbi.nlm.nih.gov/pubmed/9297984> After stating that their “greatest concern is the magnitude of exposure to organochlorines to which infants and children are subjected through human and dairy milk,” the authors continued, “the estimated intake of DDT by infants was at least 100 fold greater than the ADI (acceptable daily intake) of the FAO/WHO.” The authors were referring in that statement to infants in developing countries, but if infants in developed countries are breastfed by mothers who eat fish and shrimp, those infants are probably also subject to substantial exposures to DDT or other organochlorine pesticides from seafood consumed by their mothers. (Remember from above that about 90% of seafood consumed in the U.S. is imported, and to a large extent imported from China and its neighbors.)
It doesn’t require a high concentration of pesticides in water to raise the concentrations in fish to high levels. It is relevant to look at “bioconcentration factors” in fish for dicofol, which was one of the two pesticides most used in the fields in the area of the Roberts et al. study above, and is still in use in the U.S. as of 2015. (The bioconcentration factor in this case is the concentration of a substance in the fish in relation to its concentration in the surrounding water.http://www.epa.gov/ocspp/pubs/frs/publications/OPPTS_Harmonized/850_Ecological_Effects_Test_Guidelines/Drafts/850-1730.pdf) Three common species of fish have been found to have bioconcentration factors for dicofol of 6,100 to 25,000.Item 4 in Working group on dicofol under the POPs Review Committee of the Stockholm Convention: Dicofol, 2nd Draft Risk Profile, at http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=21&ved=0CB0QFjAAOBRqFQoTCImv9qbA8cYCFccyiAodmlkMgA&url=http%3A%2F%2Fchm.pops.int%2FPortals%2F0%2Fdownload.aspx%3Fd%3DUNEP-POPS-POPRC10CO-draftRP-Dicofol-20150320.En.doc&ei=Yv-wVYn2IcfloASas7GACA&usg=AFQjCNH8vtzEAnfGFQmd-6omqY7AaeG7jg&sig2=DMwWTQHgsP-eiCYqFmi8pg Those are increases in concentration that apparently result from the fish merely existing in water with low concentrations of pesticides, not counting the additions from pesticides contained in the food consumed by the fish.
People should not feel protected from pesticides in seafood by means of FDA inspections. In a report by the U.S. Government Accountability Office about FDA inspections of imported seafood, it was pointed out that “in fiscal year 2009, FDA tested about 0.1 percent of all imported seafood products for drug residues” (that is one out of 1,000); and this entire large report said nothing about testing for pesticides, United States Government Accountability Office: GAO-11-286, Seafood Safety: FDA Needs to Improve Oversight of Imported Seafood and Better Leverage Limited Resources, Report to Congressional Requesters: April 2011, at http://www.gao.gov/assets/320/317734.pdf even though that would have been logically closely related to inspection for other hazardous substances. Similarly, in over 4000 words of testimony to Congress in 2008 entitled, “Chinese Seafood Imports,” a deputy director of the FDA made no mention whatever of the words “pesticide” or “insecticide;” by comparison, “drug” or “drugs” was said 17 times, along with multiple references to each of various specific drugs.U.S. Food & Drug Administration, Testimony, Chinese Seafood Imports, Statement of Don Kraemer, Deputy Director, Office of Food Safety, U.S. Food and Drug Administration, before U.S. and China Economic and Security Review Commission, April 25, 2008 accessed at http://www.fda.gov/newsevents/testimony/ucm115243.htm Aside from that, a July, 2015 search on the FDA’s website for “inspection of seafood imports” brings up the following relevant results:
a) Other Congressional testimony about “Safety of Chinese Imports” that mentioned “drug” or “drugs” 24 times but did not mention pesticides even once.U.S. Food & Drug Administration, Testimony, Safety of Chinese Imports, Statement of Murray M. Lumpkin, M.D., Deputy Commissioner for International and Special Program before the Senate Committee on Commerce, Science & Transportation July 18 , 2007 at http://www.fda.gov/newsevents/testimony/ucm110728.htm
b) A 2008 statement by the FDA reported examining or sampling 1.2% of seafood imports in FY 2007; “drug” or “drugs” is mentioned 73 times, and pesticides are mentioned only two times (presumably in regard to checking for only six pesticides -- see below). FDA, Protecting and Promoting Your Health, Enhanced Aquaculture and Seafood Inspection, Report to Congress, November 20, 2008, Andrew C. von Eschenbach, M.D., Commissioner of Food and Drugs, at http://www.fda.gov/food/guidanceregulation/guidancedocumentsregulatoryinformation/seafood/ucm150954.htm
c) Testimony from 1996, in which the only specifics regarding inspection for pesticides were about non-binding “action levels” for six pesticides, with no mention of any rejection of imports because of pesticides.<Statement of Michael Friedman, M.D., Deputy Commissioner for Operations before the Subcommittee on Livestock, Dairy, and Poultry, House Committee on Agriculture, May 22, 1996. (Note that the FDA in 2002 listed 266 detectably different pesticides; FDA: Food and Drug Administration Pesticide Program Residue Monitoring 2002, at http://www.fda.gov/downloads/food/foodborneillnesscontaminants/ucm126088.pdf ) compare that with the six that the FDA tested for, and remember that even that testing for six pesticides was done for only an extremely small percentage of shipments.)
Implying surprise at the low level of rejection of Chinese food imports by the FDA, a U.S. Department of Agriculture report acknowledges, “problems like unsafe pesticide residues and heavy metal contamination could be more prevalent than indicated by FDA violations….Pesticide residues and heavy metal contaminants have been a major concern in China’s exports to Japan and Hong Kong and in produce sold in China’s domestic market.” (p. 18) So, as implied by a document of the U.S. Department of Agriculture, American consumers are likely not to be receiving the same protection against excess levels of pesticides that residents of Japan, Hong Kong and China receive. More basically, judging also by a document of another federal agency (the GAO, see above), Americans may not be receiving any significant protection from pesticides in seafood imports.
Glossing over pesticides in imported farmed fish might at first seem reasonable, considering that pesticides are not normally thought of as being intentionally added to aquaculture water and fish food. But, in countries (such as China) where pesticides are still very much part of the environment (including ones such as DDT that are illegal in the U.S.), presence of persistent pesticides in water supplies and in fish food could be quite normal. Remember that a 1997 study (Kannan et al.30) estimated intake of DDT by infants in Southeast Asian countries to be at least 100 fold greater than the acceptable daily intake recommended by WHO.
Appendix B: Biological details and other information about harm to the brain caused by newer pesticides:
As stated in a 2006 study, “The pesticides most commonly used in agriculture are organophosphorus compounds (OPCs)…. Studies carried out employing chronic exposure of animals to low doses of the OPC Dursban (chlorpyrifos) during pregnancy or just after birth showed a reduction in the manufacture of DNA and the number of cells in the brain of the fetus and the newborn (Chakraborti et al., 1993). This suggests that the nervous system of the fetus and the very young is several-fold more susceptible than the nervous system of a mature adult to such low-dose exposure.”. <<De Silva et al., Toxicity due to organophosphorus compounds: what about chronic exposure? 0035-9203/$ — Oxford Journals, Medicine and Health, Transactions RSTMH, Vol. 100, Issue 9, pp. 803-806 doi:10.1016/j.trstmh.2006.05.001, at http://trstmh.oxfordjournals.org/content/100/9/803.full.pdf+html
In a chapter of a textbook about pesticides, in which the authors draw on over 160 studies that they cite, they state (in Section 16.13), “the best studied pesticide, CPF (chlorpyrifos), is capable of disrupting every single stage of nervous system development including neuronal cell proliferation and differentiation, axonogenesis, synaptogenesis, and apoptosis.” Satoh and Gupta, Ed., Anticholinesterase Pesticides: Metabolism, Neurotoxicity, and Epidemiology, Chapter 16 (Flaskos et al, “Developmental Neurotoxicity of Anticholinesterase Pesticides.”
A team of six scientists, in a 2011 study, pointed out that ten different pesticides are known to reduce thyroid hormone levels. <Mnif et al., Effect of Endocrine Disruptor Pesticides: A Review, Int J Environ Res Public Health. 2011 Jun; 8(6): 2265–2303. PMCID: PMC3138025 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138025/ Adequate thyroid hormone is authoritatively recognized to be crucial to proper development of the brain in the early postnatal period. (Hauser et al., Resistance to Thyroid Hormone: Implications for Neurodevelopmental Research on the Effects of Thyroid Hormone Disruptors, Toxicol Ind Health January 1998 vol. 14 no. 1-2 85-101at http://tih.sagepub.com/content/14/1-2/85.abstract. Also, “Thyroid Hormone Disruption: Dioxins Linked To Attention Deficit, Learning Problems,” Jan. 13, 1998, Science Daily, http://www.sciencedaily.com/releases/1998/01/980113155609.htm; Also EPA statement in 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD); CASRN 1746-01-6 at http://www.epa.gov/iris/subst/1024.htm, from which the following is quoted: “For TCDD, the toxicological concern is… increased metabolism and clearance of the thyroid hormone, thyroxine (T4). Adequate levels of thyroid hormone are essential in the newborn and young infant as this is a period of active brain development (Zoeller and Rovet, 2004; Glinoer and Delange, 2000). Thyroid hormone disruption during pregnancy and in the neonatal period can lead to neurological deficiencies, particularly in the attention and memory domains (Oerbeck et al., 2005).”
Chlorpyrifos, a widely-used organophosphate pesticide, “works by blocking an enzyme which controls messages that travel between nerve cells. When the enzyme is blocked, the nervous system can't send normal signals.” (National Pesticide Information Center, Chlorpyrifos General Fact Sheet, at http://npic.orst.edu/factsheets/chlorpgen.html)
A metabolite of dicofol (p,p’-DCBP) has been found to have potent anti-androgen activity, in two studies. Item 7 and item 129 in Working group on dicofol under the POPs Review Committee of the Stockholm Convention: Dicofol, 2nd Draft Risk Profile, at http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=21&ved=0CB0QFjAAOBRqFQoTCImv9qbA8cYCFccyiAodmlkMgA&url=http%3A%2F%2Fchm.pops.int%2FPortals%2F0%2Fdownload.aspx%3Fd%3DUNEP-POPS-POPRC10CO-draftRP-Dicofol-20150320.En.doc&ei=Yv-wVYn2IcfloASas7GACA&usg=AFQjCNH8vtzEAnfGFQmd-6omqY7AaeG7jg&sig2=DMwWTQHgsP-eiCYqFmi8pg This should be born in mind in relation to the facts that (a) testosterone (an androgen) is known to be important to the development of the brain, (b) prevalences of both ASD and ADHD are several times as high among males as among females, and (c) as mentioned earlier, dicofol has been widely used in China and the U.S. and was one of the two pesticides most used in the fields in the area of the Roberts et al. study above.
Appendix C: The AAFP’s ignoring of research of the last two decades
The breastfeeding position paper of the American Academy of Family Physicians (http://www.aafp.org/about/policies/all/breastfeeding-support.html) does briefly address the issue of the (undeniable) presence of toxins in breast milk, saying “it is important to understand that infant formula (primarily cow’s milk and soy) also contain many of the same toxins…. By using formula, they do not reduce exposure to environmental toxins.” It is safe to say that the above is a false statement. They say nothing about the fact that human milk has been authoritatively found to typically contain several recognized developmental toxins in concentrations scores of times higher than in infant formula, and at levels far exceeding officially established safe doses. By comparison, infant formula has apparently not been found to contain any toxins at levels exceeding established safe levels. (see Section 3 of www.pollution-effects.info/) The AAFP continues, “The risk of cancers and less-than-optimal neurologic development remains higher in formula-fed babies compared with breastfed babies in similar environments.” The only verification that they offer for these statements consists of two publications that are 20 or more years old. When the author of this article has written, repeatedly, to both the AAP and the AAFP briefly presenting some of the evidence that has been developed during the past two decades, contradicting their positions, neither of those organization has ever responded. In an article that the AAFP refers to in support of its position (by Frank and Newman, Breastfeeding in a polluted world, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1485262/pdf/cmaj00269-0035.pdf), the authors state that “Until further evidence is available, physicians should continue to encourage breast-feeding because of its considerable benefits.” That recommendation was published in 1993, based on a 1991 presentation, and very considerable contradictory evidence has become available over the succeeding decades. In 2013 and 2014, when authoritative post-1991 studies were repeatedly brought to their attention with findings adverse to breastfeeding, the AAFP (like the AAP) has no response. Neither organization acknowledges awareness of the dozens of peer-reviewed, published scientific studies that have found adverse effects of breastfeeding, after repeatedly being informed about them, much less do they have any response to them. But they continue to hold and tell doctors to hold a position that ignores the contrary studies.
Appendix D: Distinctly postnatal vulnerability of the developing brain to exposures to pesticides, including the newer ones, continued:
Basic information on this topic has already been presented in Section 1.b, item b. In addition,
- A 2008 study in an Oxford journal reported about neurological effects of postnatal exposures (as measured in urine samples) and stated that its own findings “add important information to the limited body of knowledge about the (adverse) effects of OP (organophosphate) pesticide exposure on children's cognitive functioning;” the authors cited many other studies with compatible results, including studies with findings specifically of effects of postnatal exposures.(Lizardi et al., The Effects of Organophosphate Pesticide Exposure on Hispanic Children's Cognitive and Behavioral Functioning, Oxford Journals, Journal of Pediatric Psychology, (2008) Vol. 33 Issue 1, at http://jpepsy.oxfordjournals.org/content/33/1/91.long)
-- Several of the studies cited in the Jurewicz et al. 2013 review article that studied effects of exposures to pesticides (Jurewicz et al., Chemical exposure early in life and the neurodevelopment of children – an overview of current epidemiological evidence, Annals of Agricultural and Environmental Medicine 2013, Vol 20, No 3, 465–486, at http://www.ncbi.nlm.nih.gov/pubmed/24069851 (Lizardi et al., 2008, Eskenazi et al., 2007, Ruckart et al., 2007) were specifically finding effects of postnatal exposures. Other studies, which stated their findings only in relation to prenatal exposures, could very well have actually been finding effects of early postnatal exposures via breastfeeding, since they did not measure exposures during the developmentally-critical early months after birth.<<see www.autism-research.net/postnatal-effects.htm>>.
-- Metabolites (“DEs” specifically) of certain types of organophosphate pesticides were found in a 2007 study to be associated with pervasive development disorder (PDD) in relation to postnatal but not prenatal exposure. (PDD is the general category of disorders of which autism is a subclass.) Other metabolites were found to be associated with PDD both prenatally and postnatally.Eskenazi and seven others, Organophosphate Pesticide Exposure and Neurodevelopment in Young Mexican-American Children, Environ Health Perspect. 2007 May; 115(5): 792–798. PMCID: PMC1867968, Table 5, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1867968/
-- Odds of PDD approximately doubled with a 10-fold increase in children’s levels of metabolites of organophosphate pesticides; Center for Environmental Research and Children’s Health, UC Berkeley School of Public Health: Organophosphate Pesticide Exposure and Neurodevelopment in Young Mexican-American Children, at http://cerch.org/organophosphate-pesticide-exposure-and-neurodevelopment-in-young-mexican-american-children/ 10-fold may sound like an unusually large increase, but it is not; good evidence indicates it to be merely the difference between the 25th and 75th percentiles of children's concentrations of organophosphate pesticides. Bouchard et al., Attention-Deficit/Hyperactivity Disorder and Urinary Metabolites of Organophosphate Pesticides, Pediatrics, Vol. 125 No. 6 June 1, 2010, pp. e1270 -e1277 at http://pediatrics.aappublications.org/content/125/6/e1270.full That very common difference in exposure to background levels of organophosphate pesticides was associated with doubling of risk of PDD.
-- A 2015 study found that “Children with urinary 3-PBA (a metabolite of the pesticide, pyrethroid) above the limit of detection (LOD) were twice as likely to have ADHD compared with those below the LOD (adjusted odds ratio [aOR] 2.42.)”Wagner-Schuman and 7 others, Association of pyrethroid pesticide exposure with attention-deficit/hyperactivity disorder in a nationally representative sample of U.S. children, Environ Health. 2015; 14: 44. PMCID: PMC4458051 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458051/
-- “Concerns have been raised that the developing brain may be particularly vulnerable to adverse effects of neurotoxic pesticides.” (For considerable evidence of major postnatal development of the brain, see www.disability-origins.info.) Continuing to quote from the same authors, “Laboratory experimental studies suggest that many pesticides … can cause neurodevelopmental toxicity. Adverse effects on brain development can be severe and irreversible.”Bjorling-Poulsen et al., Potential developmental neurotoxicity of pesticides used in Europe, Environ Health. 2008; 7: 50. PMCID: PMC2577708 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577708/
-- According to a policy statement of the American Academy of Pediatrics (accessed July, 2015), animal experiments as well as human epidemiologic evidence “demonstrate associations between early life exposure to pesticides and pediatric cancers, decreased cognitive function, and behavioral problems.” Continuing, “the evidence base is most robust for associations to pediatric cancer and adverse neurodevelopment.” (Policy Statement, Pesticide Exposure in Children, Council on Environmental Health, American Academy of Pediatrics, http://pediatrics.aappublications.org/content/130/6/e1757.long
*As the author of the above, my role has not been carrying 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 into a form that enables readers to make better-informed decisions about related matters. The original research articles and government reports on this subject are extremely numerous, typically very lengthy, and usually written in a form and stored in a location such that the general public is 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 diverse, authoritative sources and to summarize it into a form that is reasonably understandable to the general public, while maintaining excellent accuracy in presentation of the evidence. 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 you 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. That approach is especially relevant to the position statements on breastfeeding of the American Academy of Pediatrics and the American Academy of Family Physicians, which statements cite only evidence that has been
(a) selected, while in no way acknowledging the considerable contrary evidence(1) and
(b) of a kind that has been authoritatively determined to be of low quality; former U.S. Surgeon General Regina Benjamin acknowledged that essentially all of the research supporting benefits of breastfeeding consists merely of observational studies.(1a) One determination that evidence from observational studies is of low quality has been provided by Dr. Gordon Guyatt and 14 of his associates;(2) Dr. Guyatt is chief editor of the American Medical Association’s Manual for Evidence-based Clinical Practice, in which 26 pages are devoted to examples of studies (most of which were observational) that were later found to be wrong by high-quality studies.(2a) A similar assessment of the low quality of evidence from observational studies has been provided by the other chief authority on medical evidence (Dr. David Sackett),(2c) writing about “the disastrous inadequacy of lesser evidence,” in reference to findings from observational studies.(2b)
When a brief summary of material that conflicts with their breastfeeding positions is repeatedly presented to the physicians’ associations, along with a question or two about the basis for their breastfeeding recommendations, those associations never respond. That says a lot about how well their positions on breastfeeding can stand up to scrutiny.
The credibility of the contents of the above article is based on the authoritative sources that are referred to in the footnotes: The sources are mainly U.S. government health-related agencies and reputable academic researchers (typically highly-published authors) writing in peer-reviewed journals; those sources are essentially always referred to in footnotes that follow anything that is said in the text that is not common knowledge. In most cases a link is provided that allows easy referral to the original source(s) of the information. If there is not a working link, you can normally use your cursor to select a non-working link or the title of the document, then copy it (control - c usually does that), then “paste” it (control - v) into an open slot at the top of your browser, for taking you to the website where the original, authoritative source of the information can be found.
The reader is strongly encouraged to check the source(s) regarding anything he or she reads here that seems to be questionable, and to notify me of anything said in the text that does not seem to accurately represent what was said by the original source. Write to email@example.com. I will quickly correct anything found to be inaccurate.
For a more complete statement about the author and Pollution Action, please go to www.pollutionaction.org.
1) EM Roberts et al., Maternal residence near agricultural pesticide applications and autism spectrum disorders among children in the California Central Valley, Environ Health Perspect. 2007 Oct;115(10):1482-9, at http://www.ncbi.nlm.nih.gov/pubmed/17938740/ “comparing children of mothers living within 500 m of field sites with the highest nonzero quartile of organochlorine poundage to those with mothers not living near field sites suggested an odds ratio for ASD of 6.1 (95% confidence interval, 2.4-15.3”
2) Weldon et al., A pilot study of pesticides and PCBs in the breast milk of women residing in urban and agricultural communities of California, Journal of Environmental Monitoring, DOI: 10.1039/c1em10469a, at http://ehsdiv.sph.berkeley.edu/holland/publications/files/Weldon2011.pdf Also, Non-persistent Pesticides Found in U.S. Mothers' Breast Milk, Bridges, Spring 2012, Regents of the University of California, Center for Occupational and Environmental Health, at http://coeh.berkeley.edu/bridges/Spring2012/PesticidesBM.html
3) Roberts and English, Bayesian modeling of time-dependent vulnerability to environmental hazards: an example using autism and pesticide data, Statistics in Medicine, Published online 7 September 2012 in Wiley Online Library (wileyonlinelibrary.com) DOI: 10.1002/sim.5600)
4) Pesticides in the Diets of Infants and Children, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C. 1993, p. 25 at http://www.nap.edu/openbook.php?record_id=2126&page=43
5) Bjorling-Poulsen et al., Potential developmental neurotoxicity of pesticides used in Europe, Environ Health. 2008; 7: 50. PMCID: PMC2577708 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577708/
6) Needham et al., Partition of Environmental Chemicals between Maternal and Fetal Blood and Tissues, Environ Sci Technol. Feb 1, 2011; 45(3): 1121–1126, Table 2, at http://pubs.acs.org/doi/pdf/10.1021/es1019614
7) Eskenazi et al., PON1 and Neurodevelopment in Children from the CHAMACOS Study Exposed to Organophosphate Pesticides in Utero, Environ Health Perspect. 2010 Dec; 118(12): 1775–1781. PMCID: PMC3002199 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3002199/; and Eskenazi and seven others, Organophosphate Pesticide Exposure and Neurodevelopment in Young Mexican-American Children, Environ Health Perspect. 2007 May; 115(5): 792–798. PMCID: PMC1867968 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1867968/; the lowest reported breastfeeding percentage, 95%, was found in Weldon et al., Serum Persistent Organic Pollutants and Duration of Lactation amongMexican-AmericanWomen>, Journal of Environmental and Public Health Volume 2010, Article ID 861757, at http://ehsdiv.sph.berkeley.edu/holland/publications/files/Weldon2011.pdf
8) Nair et al., DDT and HCH Load in Mothers and Their Infants in Delhi, India, Bulletin of Environmental Contamination and Toxicology, Volume 56, Issue 1 , pp 59 at http://link.springer.com/article/10.1007%2Fs001289900009?LI=true#page-1
9) Kanja et al., A comparison of organochlorine pesticide residues in maternal adipose tissue, maternal blood, cord blood, and human milk from mother/infant pairs, Archives of Environmental Contamination and Toxicology, January 1992, Volume 22, Issue 1, pp 21-24 at http://link.springer.com/article/10.1007/BF00213297#page-1
Radomski et al., Blood levels of organochlorine pesticides in Argentina: Occupationally and nonoccupationally exposed adults, children and newborn infants, Toxicology and Applied Pharmacology, Volume 20, Issue 2, October 1971, Pages 186–193, at http://www.sciencedirect.com/science/article/pii/0041008X719004451900445
.Saxena et al., Placental Transfer of Pesticides in Humans, Arch Toxicol (1981) 48:127-134, at http://repository.ias.ac.in/29356/1/308.pdf
10) Eyster et al., Partitioning of polybrominated biphenyls (PBBs) in serum, adipose tissue, breast milk, placenta, cord blood, biliary fluid, and feces, Arch Environ Health, 1983 Jan-Feb;38(1):47-53. at http://www.ncbi.nlm.nih.gov/pubmed/6299210. A less extreme lactational-to-fetal PBB exposure ratio (12 to 1) was found in a 1984 study that tested 138 mother-infant pairs. Jacobson et al., The Transfer of Polychlorinated Biphenyls (PCBs) and Polybrominated Biphenyls (PBBs) Across the Human Placenta and into Maternal Milk, 1984 American Journal of Public Health 0090-0036/84 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1651484/pdf/amjph00627
11) ATSDR’s Toxic Substances Portal - Polybrominated Biphenyls (PBBs) & Polybrominated Diphenyl Ethers (PBDEs) at http://www.atsdr.cdc.gov/PHS/PHS.asp?id=527&tid=94
12) Their use in China in electronic products was discontinued in 2007,”China making environmentally-friendly standards for electronic products,” May 17, 2006, People’s Daily Online, at http://en.people.cn/200605/17/eng20060517_266339.html but apparently it was continued in textiles and cushioning, which are widely imported from China.
13) Terrell et al., A cohort study of the association between secondary sex ratio and parental exposure to polybrominated biphenyl (PBB) and polychlorinated biphenyl (PCB), Environmental Health, 2009, at http://www.ehjournal.net/content/8/1/35
14) Lackmann et al., [Lactational transfer of presumed carcinogenic and teratogenic organochlorine compounds within the first six months of life], Z.Geburtshilfe Neonatal, 2005 Oct;209(5):186-91.at http://www.ncbi.nlm.nih.gov/pubmed/16317629
15) Lackman et al., Organochlorine compounds in breast-fed vs. bottle-fed infants: preliminary results at six weeks of age, Sci Total Environ., 2004 Aug 15;329(1-3):289-93, at http://www.ncbi.nlm.nih.gov/pubmed/15262173
16) Fig. 3 of Gascon and eight others: Temporal trends in concentrations and total serum burdens of organochlorine compounds from birth until adolescence and the role of breastfeeding, Environment International, Volume 74, January 2015, Pages 144–151, at http://www.sciencedirect.com/science/article/pii/S0160412014003043 )
Banning DDT in Spain in 1977: Zumbado et al., Inadvertent exposure to organochlorine pesticides DDT and derivatives in people from the Canary Islands (Spain), Science of the Total Environment 339 (2005) 49– 62, 2004,
17) 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
18) Damgard and eight others, Persistent Pesticides in Human Breast Milk and Cryptorchidism, Environ Health Perspect. 2006 Jul; 114(7): 1133–1138. Table 2, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1513324/table/t2-ehp0114-001133/
19) Weldon et al., A pilot study of pesticides and PCBs in the breast milk of women residing in urban and agricultural communities of California, Journal of Environmental Monitoring, DOI: 10.1039/c1em10469a, at http://ehsdiv.sph.berkeley.edu/holland/publications/files/Weldon2011.pdf Also, Non-persistent Pesticides Found in U.S. Mothers' Breast Milk, Bridges, Spring 2012, Regents of the University of California, Center for Occupational and Environmental Health, at http://coeh.berkeley.edu/bridges/Spring2012/PesticidesBM.html
20) Pesticides in the Diets of Infants and Children, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C. 1993, p. 232
21) USDA, Pesticide Data Program, Annual Summary, 2013, Appendix L, at http://www.ams.usda.gov/sites/default/files/media/2013%20PDP%20Anuual%20Summary.pdf
22) This 2011 study examined many different “exposure prediction factors” that could contribute to children’s levels of metabolites of organophosphorous pesticides and found that, at six months of age, current breastfeeding was a stronger predictor of exposures to this major group of pesticide types than eleven other factors considered. The only factors that were stronger predictors (residence or child care less than 60 meters from an agricultural field and home use of pesticides during the previous six months) applied to only a small minority of all children studied (10% or less); therefore, for the vast majority of young infants, current breastfeeding was found to be THE strongest predictor of their levels of exposure to a major group of pesticides, among the many possibilities that were considered. Bradman et al., Determinants of Organophosphorus Pesticide Urinary Metabolite Levels in Young Children Living in an Agricultural Community, International Journal of Environmental Research and Public Health ISSN 1660-4601, Table S-4, at http://www.mdpi.com/1660-4601/8/4/1061
23) Adamović et al., Some observations concerning the ratio of the intake of organochlorine insecticides through food and amounts excreted in the milk of breast-feeding mothers, Bull. Environm. Contam. Toxicol. 20, 280-285 (1978), http://link.springer.com/article/10.1007%2FBF01683521?LI=true#page-1)
24) Grandjean and Jensen, Breastfeeding and the Weanling’s Dilemma Am J Public Health. 2004 July; 94(7): 1075. PMCID: PMC1448391 at www.ncbi.nlm.nih.gov/pmc/articles/PMC1448391
25) Dioxins, PCBs and mercury have long been recognized to be neurodevelopmental toxins. PBDEs have more recently been recognized as such: “PBDE’s are known to be endocrine disruptors and have neurologic toxicity. (Rudel, 2003)” (WHO, Persistent Organic Pollutants: Impact on Child Health, at http://whqlibdoc.who.int/publications/2010/9789241501101_eng.pdf
26) Re: EPA’s RfD for dioxin: At www.epa.gov/iris/supdocs/dioxinv1sup.pdf in section 4.3.5, at end of that section, "...the resulting RfD in standard units is 7 × 10−10 mg/kg-day." (that is, O.7 pg TEQ/kg-d)
Re: breastfed infants’ exposures to dioxins, in U.S. and internationally:
- Infant Exposure to Dioxin-like Compounds in Breast Milk Lorber (Senior Scientist at EPA) et al., VOL. 110 No. 6 June 2002, Environmental Health Perspectives http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download
- Wittsiepe J, PCDD/F and dioxin-like PCB in human blood and milk from German mothers. Chemosphere. 2007 Apr;67(9):S286-94. Epub 2007 Jan 10. http://www.ncbi.nlm.nih.gov/pubmed/17217986
-Yang J, et al., PCDDs, PCDFs, and PCBs concentrations in breast milk from two areas in Korea: body burden of mothers and implications for feeding infants. Chemosphere. 2002 Jan;46(3):419-28. At www.ncbi.nlm.nih.gov/pubmed/11829398
- Bencko V et al., Exposure of breast-fed children in the Czech Republic to PCDDs, PCDFs, and dioxin-like PCBs. Environ Toxicol Pharmacol. 2004 Nov;18(2):83-90. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/21782737/
- Nakatani T, et al., Polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and coplanar polychlorinated biphenyls in human milk in Osaka City, Japan Arch Environ Contam Toxicol. 2005 Jul;49(1):131-40. Epub 2005 Jun 22. Found at http://link.springer.com/article/10.1007%2Fs00244-004-0051-y#page-1
- Deng B, et al., Levels and profiles of PCDD/Fs, PCBs in mothers' milk in Shenzhen of China: estimation of breast-fed infants' intakes.Environ Int. 2012 Jul;42:47-52.. At http://www.ncbi.nlm.nih.gov/pubmed/21531025
- Chovancová J, et al., PCDD, PCDF, PCB and PBDE concentrations in breast milk of mothers residing in selected areas of Slovakia Chemosphere. 2011 May;83(10):1383-90. doi: 10.1016/j. At www.ncbi.nlm.nih.gov/pubmed/21474162
- J Grigg, Environmental toxins; their impact on children’s health, Arch Dis Child 2004;89:244-250 doi:10.1136/adc.2002.022202 at http://adc.bmj.com/content/89/3/244.full
27) Re: RfD of PBDEs:- EPA Technical Fact Sheet on Polybrominitated Diphenyl Eithers (PBDEs) and PBBs, p.4 at http://www2.epa.gov/fedfac/technical-fact-sheet-polybrominated-diphenyl-ethers-pbdes-and-polybrominated-biphenyls-pbbs -- RfDs: 1 x 10-4 mg/kg/day (=100ng/kg/day) for the BDE 47 and 99 congeners. (Note that BDE 47 typically constitutes over half of the PBDEs present in humans. -- Daniels et al., Individual Characteristics Associated with PBDE Levels in U.S. Human Milk Samples, Environmental Health Perspectives, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831961/figure/f1-ehp-118-155/) Regarding prevalence of tetraBDEs (47), see also Costa LG, et al., Polybrominated diphenyl ether (PBDE) flame retardants: environmental contamination, human body burden and potential adverse health effects. Acta Biomed. 2008 Dec;79(3):172-83 at www.ncbi.nlm.nih.gov/pubmed/19260376.
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:
28) Re: Mercury levels in breast milk: U.S. ATSDR document on mercury at www.atsdr.cdc.gov/toxprofiles/tp46-c5.pdf, p. 443
- Re: mercury levels allowed in bottled water: Code of Federal Regulations, Title 21, Chapter 1, Subchapter B, Part 165, Subpart B, Sec. 165-110 at http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfCFR/CFRSearch.cfm?fr=165.110
29) Re: PCB levels 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)
30) Kannan et al., Organochlorine pesticides and polychlorinated biphenyls in foodstuffs from Asian and Oceanic countries, Article in Reviews Of Environmental Contamination And Toxicology · January 1997· DOI: 10.1007/978-1-4612-1964-4_1 p. 43, at http://www.researchgate.net/publication/13923281_Organochlorine_pesticides_and_polychlorinated_biphenyls_in_foodstuffs_from_Asian_and_Oceanic_countries._Rev_Environ_Cont_Toxicol
31) Re: dioxins in formula less than 1% of dioxins in breast milk:
- U.K. Food Standards Agency Food Survey Information Sheet 49/04 MARCH 2004, Dioxins and Dioxin-Like PCBs in Infant Formulae, found at http://www.food.gov.uk/multimedia/pdfs/fsis4904dioxinsinfantformula.pdf
- Compatible figures were found in Weijs PJ, et al., Dioxin and dioxin-like PCB exposure of non-breastfed Dutch infants. Chemosphere. 2006 Aug;64(9):1521-5. Epub 2006 Jan 25 at www.ncbi.nlm.nih.gov/pubmed/16442144
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)
Re: DDT in infant formula minor compared with that in human milk:
In thorough studies by two major agencies, infant formula in the U.S. was found to be almost totally free of detectable pesticide residues. (see Section 1.d) But concerns about DDT as a developmental toxin apply mainly to developing countries, where it is still widely applied.
-- DDT in human milk widely exceeding ADI in developing countries: Average in India of about 19 times the ADI (acceptable daily intake) of .005 mg/kg/day recommended by WHO. (p. 197 of Kalra et al., Pesticidal Contamination of Foods in the Year 2000 AD, Proc. Indian nain. Sci. Acad B52 No. 1 (1985) at http://184.108.40.206/rawdataupload/upload/insa/INSA_2/20005a0e_188.pdf) Also in Section 4.a, notice in the small chart that estimated average daily infant intake of DDT in Tunisia exceeds the tolerable daily intake (TDI) by 20%, and in the large chart that many countries have breast milk concentrations of DDT and its metabolites that far exceed those in Tunisia. Also a 1997 study of organochlorine pesticides in food in Asian countries, referring to “concentrations in human breast milk,” stated that “intake of organochlorines, particularly DDT, by infants in developing Asian countries was as great as 100 fold the ADI.” (p. 43 of Kannan et al., Organochlorine pesticides and polychlorinated biphenyls in foodstuffs from Asian and Oceanic countries, Article in Reviews Of Environmental Contamination And Toxicology · January 1997· DOI: 10.1007/978-1-4612-1964-4_1 p. 43, at http://www.researchgate.net/publication/13923281_Organochlorine_pesticides_and_polychlorinated_biphenyls_in_foodstuffs_from_Asian_and_Oceanic_countries._Rev_Environ_Cont_Toxicol
-- Infant formula is available that is free of DDT and free of pesticides in general, and that is apparently the way it essentially always is in the U.S. -- see Section 1.d. Some locally-produced infant formula in India has been found to contain DDT, but there does not appear to be research published comparing locally-produced infant formula with local breast milk, in developing countries.
32) Doerner et al., DDT in human milk and mental capacities in children at school age: An additional view on PISA 2000*, neuroendocrinology Letters Nos. 5/6, Oct-Dec, Vol. 23, 2002, at http://www.researchgate.net/profile/Andreas_Plagemann/publication/10975528_DDT_in_human_milk_and_mental_capacities_in_children_at_school_age_an_additional_view_on_PISA_2000/links/53d7781f0cf29265323cc680.pdf
33) Nair et al., DDT and HCH Load in Mothers and Their Infants in Delhi, India, Bulletin of Environmental Contamination and Toxicology, Volume 56, Issue 1 , pp 59 at http://link.springer.com/article/10.1007%2Fs001289900009?LI=true#page-1
34) Some observations concerning the ratio of the intake of organochlorine insecticides through food and amounts excreted in the milk of breast-feeding mothers, Bull. Environm. Contam. Toxicol. 20, 280-285 (1978), http://link.springer.com/article/10.1007%2FBF01683521?LI=true#page-1)
35) 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
36) Fig. 3 of NRDC statement at http://www.nrdc.org/breastmilk/chems.asp
37) Bennetto et al., Children with autism spectrum disorder have reduced otoacoustic emissions at the 1 kHz mid-frequency region, Autism Research, at http://onlinelibrary.wiley.com/doi/10.1002/aur.1663/abstract. Also an article in Medline Plus, Aug. 1, 2016, R. Preidt,"Hearing Test May Predict Autism Risk Sooner: Study" at https://medlineplus.gov/news/fullstory_160181.html