http://www.autism-research.net/image001.gif 

 

 

Recent Research related to Autism, and

Connections with Widespread Environmental Toxins

 

Contents:

Introduction:  Developmental toxins to which infants are widely exposed at high levels

 

Section 1:  Why autism rates were stable in the U.K. while they were growing rapidly in the U.S.

 

Section 2:  Autism incidence declines with birth order, in parallel with declines in exposure to developmental toxins in breast milk by birth order:

 

Section 3:  Autism linked to dysfunction of the cerebellum, which is especially vulnerable to toxins during the year after birth:

 

Section 4:  Eye contact normal shortly after birth, then declining as environmental toxins in the infant’s body increase greatly and continue accumulating

 

Section 5:  Trends related to the increase of autism

 

Section 6:  Studies finding autism-related effects of relatively commonly-present concentrations of these toxins

 

Section 7:  Studies specifically relating autism incidence to breastfeeding

 

Section 8:  Questions that logically come up in relation to the above

 

Introduction

During the last half century or so, toxins that have become widespread in the environment have also become substantial contaminants in human milk.1   Breast milk in contemporary developed countries now includes four neuro-developmental toxins1a at levels greatly exceeding governmentally-established thresholds for safety:  

(a) dioxins, exceeding the EPA’s Reference Dose (estimated reasonably safe dose, or RfD) by scores to hundreds of times;2  

(b) PBDEs, normally well above and up to 20 times the EPA’s RfD;2a  

(c) mercury, typically four times the maximum allowed by U.S. law in bottled water, but in many cases much higher than that;2b and

(d) PCBs, in human milk in concentrations about 20 times the maximum allowed by law in U.S. public water supplies.2c 

 

 

All four of the above are present in infant formula in concentrations less than 4% as high, and usually less than 1% as high, as their concentrations in human milk.3a

 

All of the above as well as what follows is accurately based on statements from authoritative sources, which are referred to in the footnotes.

 

  According to experts on the subject (in line with statements by several other authorities), "Significantly more (10 to 20 times) of a mother's body burden of persistent organohalogens is transferred to the infant via the milk than by the transplacental route."3b  Note that persistent organohalogens include dioxins, PCBs and PBDEs, three of the neurodevelopmental toxins itemized just above. According to the U.S. Agency for Toxic Substances and Disease Registry,breast milk exposures (to PCBs) have been associated with neurodevelopmental deficits in newborn and young children.”3c

 

Substantially increasing the effects of the above concentrations, breastfeeding became far more prevalent in the U.S. after 1971, and that upward trend is continuing today.3  

 

 

Section 1:  Why autism rates were stable in the U.K. while they were growing rapidly in the U.S.:

 

Recent trends in autism prevalence in the U.K. compared with prevalence in the U.S. provide evidence of a causal link with the recently-increased toxins in human milk.  In Autism Speaks’ Oct. 16 Science News article, “Study Finds Autism Prevalence Has Leveled Off in United Kingdom,” it was stated that reported prevalence of autism in the U.K. was stable from 2004 to 2010, in contrast with continuing rapid growth of ASD prevalence in the U.S.4  We should look at breastfeeding data that would apply to the years of the infancies of the (8-year-old) children whose autism prevalence was recorded, therefore ideally finding data for the years 1996 to 2002.  For the U.K., the closest years for which there are data are 1995 to 2000.  According to the UK's National Health Service, “the prevalence of breastfeeding at later ages (referring in this case to all breastfeeding past initial breastfeeding in the hospital) did not increase between 1995 and 2000.”5   After those years of stable breastfeeding, the first data point at which an increase is shown is 2005.  So, during the general period of the infancies of the U.K. children whose autism rates were not increasing, breastfeeding was basically level.

 

That same October 16 article points out that there was a large increase in estimated prevalence of autism in the U.S. between 2002 and 2008.  Since the prevalence discussed applied to 8-year-olds, the most relevant years of U.S. infant exposures to toxins would have been 1994 to 2000.  During that brief time interval, breastfeeding at 6 months in the U.S. increased 34%.6 

 

To sum up:  In the U.K., no increase in autism rates among children born during the period when breastfeeding rates were not increasing in that country.  In the U.S. by contrast, large increase in autism prevalence among children born when there were ongoing rapid increases in breastfeeding rates.

 

Another development that seems surprising initially, until one thinks about what could explain what is happening, follows:

 

Section 2:  Autism incidence declines with birth order, in parallel with declines in exposure to developmental toxins in breast milk by birth order:

 

A typical fourth child’s risk of autism is half as high as that of a firstborn.  The odds of being diagnosed with autism decrease progressively from first to 2nd-, 3rd-, and 4th-born children.8  Infants later in birth order  (a) are less likely to be breastfed,9a (b) are breastfed for shorter periods on average,9b and (c) the milk they receive has toxin levels that have been reduced as a result of excretion to earlier-born infants during previous breastfeeding.9c

 

Could later-born children conceivably benefit from the greatly reduced exposure to toxins in breast milk?

 

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Breast milk (with its undisputed content of at least four neuro-developmental toxins, in doses scores of times higher than in formula) is consumed during the time period when harmful effects leading to autism are very likely to be taking place; most of the brain’s growth and a large part of its development takes place during the first year after birth.(see chart and footnote 10)     According to EPA researchers as well as a publication of the National Academy Press, an organ is generally at its greatest vulnerability to environmental toxicants if exposure to the toxins occurs during development of that organ.11, 11a

 

There is a widespread assumption that vulnerability of infant development to effects of environmental toxins takes place prenatally rather than postnatally.  That assumption is probably valid in relation to certain toxins, but it is not at all valid in relation to others, according to the highest authorities and according to many scientific studies.  For considerable information on this topic, go to www.autism-research.net/postnatal-effects.htm. 

 

Remember that in recent decades, while autism has been increasing, there have been dramatic increases in both breastfeeding rates and in pollutants in breast milk.

 

Section 3:  Autism linked to dysfunction of the cerebellum, which is especially vulnerable to toxins during the year after birth:

 

A 2013 study in the NIH’s National Library of Medicine reported on “converging findings from human postmortem research, human neuroimaging studies, and animal models…. Evidence appears to support cerebellar dysfunction… as a contributor to the autism phenotype.12   Remembering the special vulnerability of an organ to toxins during development of the organ, consider that about 80% of the cerebellum’s growth apparently takes place during the first year after birth (see chart),13  which is to say that this autism-linked brain region’s greatest vulnerability to toxins occurs during the period when breastfed infants are receiving extraordinarily high doses of developmental toxins.

 

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One of the forms of mercury that is widely present in human milk (due to its increasing presence in fish and seafood), methylmercury, is one of the “environmental agents with the property of killing neurons as they are born,” according to a study referred to by the NIH.11  In an experiment, rats exposed to methylmercury on postnatal day 7 were found to have brain cell death induced by a single exposure to that chemical at a level estimated to be chronic for many humans14   A 2006 study determined that, of the three sources of infant mercury exposure, ingestion (breast milk), inhalation, and dermal exposure, the largest contribution was from breast milk, providing 96 to 99.6% of the total exposure.15     Authoritative studies have found that mercury concentrations in infants that had been breastfed for six months or one year were two or three times as high as in bottle-fed infants.18

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Section 4:  Eye contact normal shortly after birth, then declining as environmental toxins in the infant’s body increase greatly and continue accumulating

In a 2013 study dealing with “this basic mechanism of social adaptive action” among infants who were later diagnosed with ASD, the researchers found that the infants started out with normal eye contact as of their first two months after birth; then a decline in eye contact began and continued steadily downward.  This decline following initial normalcy was seen by the researchers to represent a “derailment” of a social developmental process that had initially been satisfactory.16  Seeing this distinctly postnatal transition from good to bad, taking place while the infant’s brain is going through its period of greatest vulnerability to toxins (see above), we should think about any toxic exposures that are known to take place shortly before that derailment. Of special interest are toxic exposures that (a) have effects widely in the population, and (b) continue as the decline continues:

   1) Remember from the introduction that dioxins in breast milk typically exceed the EPA’s RfD by scores to hundreds of times; a German study found that, by 11 months of age, dioxin toxicity-equivalent concentrations in the breastfed infants had become 10 times higher than in formula-fed infants.17

     2) Remember that PBDEs in breast milk are normally well above but have been found to be up to tens of times the EPA’s RfD.

   3) Remember that PCBs in human milk are typically about 20 times the level allowed in U.S. public water supplies and that, according to the ATSDR,breast milk exposures (to PCBs) have been associated with neurodevelopmental deficits in newborn and young children.”3c

   4) Note again that mercury in breast milk averages about four times the maximum allowed by U.S. law in bottled water, and that studies have found mercury in infants breastfed for a year to be three times as high as in bottle-fed infants.18  In addition to this extraordinarily high general presence in breastfed infants, note also that mercury has been found to accumulate in the brain, reaching levels seven times the levels in blood.18a  All that should be born in mind along with knowledge of mercury’s “property of killing neurons as they are born.”11

 

Just one exposure to a neurodevelopmental toxin that greatly exceeds established safe levels would be highly significant when considering toxic effects on infants that occur shortly after birth, and which could therefore help explain the derailment that has been found to start at two months after birth.  But consider that a typical breastfed infant is subject to all four exposures,

a) each of which far exceeds established safe levels, and

b) each of which begins not long before adverse outcomes regularly start to become apparent. 

 

Section 5:  Trends related to the increase of autism:

Bear in mind the following trends related to autism’s increase:

(a) Breastfeeding was uncommon in the U.S. as of the 1960’s,19 when autism was extremely rare, and increased many times over after 1971(3)

(b) only during the last half century or so have environmental toxins become substantial contaminants in human milk;1   

(c) dioxins, although declining in human milk in some countries, were increasing in the U.S. as of the latest reports,20 and in every case still exceed governmentally-established safe levels by large multiples;  

(d) mercury, emitted by fossil fuel combustion, has increased several-fold in the environment of modern generations;21 and

(e) a study of sediment from multiple locations in the Great Lakes found that PBDE levels increased by a factor of several hundred times since the 1970s.22   PBDE concentrations in human milk in Canada were found to increase 7-fold just between 1992 and 2002.23  

 

 

Section 6:  Studies finding autism-related effects of relatively commonly-present concentrations of these toxins:  

 

   (a) A 2011 study found that 4-year-olds with higher levels of PBDEs had over 2½ times the risk of poor social competence, compared with children with lower levels of PBDEs;24  this should be seen in combination with the nearly 3-to-1 difference in levels of PBDEs in breastfed as compared with formula-fed children at age 4, as reported in what is apparently the only study that has made such a comparison.24b

   (b) At least five published studies have found high levels of mercury in the autistic.24a  (The studies that have failed to find this association have (a) focused on thimerosal, which contains only ethylmercury, one of many species of that chemical or (b) measured mercury levels in children far past the vulnerable early-postnatal period.)  The studies finding associations of autism with mercury levels less than twice the normal range should be seen together with the findings in multiple studies of doubling or tripling of infant mercury levels resulting from breastfeeding, taking place during the infant’s period of rapid brain growth.18   

     (c) A major 2013 study, analyzing data from all over the U.S., found close associations between autism prevalence and exposures of the mothers to variations of air pollution of kinds very widely present across the U.S., especially diesel emissions.27  Note that diesel emissions include dioxin, PCBs and PBDEs, and that these toxins are passed on to a breastfed infant in greatly concentrated form -- see below.

 

Such studies have sometimes been interpreted to mean that harm results from fetal exposure to toxins during gestation, but close reading of the studies reveals nothing indicating that the harm was necessarily prenatal. The effects were at least as likely to have originated from postnatal exposures, as indicated by the following:   two leading experts on toxins involved in child development (P. Grandjean and P.J. Landrigan) have stated that “Persistent lipophilic substances (which include dioxins, PCBs and PBDEs), 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. 28   So high levels of toxins, accumulated from the mother’s long-term exposures, are excreted in concentrated form to a breastfed infant during the continuing period when the brain is especially vulnerable to toxins due to its rapid growth (see earlier chart and accompanying text). 

 

Section 7:  Studies specifically relating autism incidence to breastfeeding:

-- On the basis of data from all 50 states and 51 U.S. counties, a highly-published scientist and Fellow of the American College of Nutrition found that "exclusive breast-feeding shows a direct epidemiological relationship to autism" and also that "the longer the duration of exclusive breast-feeding, the greater the correlation with autism."25  

-- Another U.S. study (Williams et al.),26 a very large Canadian study (Dodds et al.),26a and a U.K. study (Whitely et al.)26b all arrived at compatible findings. 

 

Note that all of these 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.26a  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.26b  In the Williams study, the duration of breastfeeding used for comparison was a full six months, which was associated with an approximately 185% (37/13) higher rate of autism.26  That same kind of correlation was also found in the Shamberger study, as quoted above.

 

 

For considerable other information on correlations between lactational exposures to toxins (especially mercury) and subsequent incidence of autism, see www.autism-correlations.info

 

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COMMENTS or questions:  At the next link are comments and questions from readers, including seven doctors.  Some of the doctors have been critical but others have been in agreement with us (including one with children with asthma, one who says she has delivered thousands of babies, and one with an autistic child); they put into briefer, everyday language and personal terms some important points that tend to be immersed in detail when presented in our own publications.  Also, we have responded to many readers’ questions and comments, including about having breast milk tested for toxins and about means of trying to achieve milk that is relatively free of toxins, including the “pump and dump” option.  To read the above, go to www.pollutionaction.org/comments.htm .

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Section 8:  Questions that logically come up in relation to the above:

So we have the unexpected close geographic correlations of autism prevalence with breastfeeding rates, plus the surprising stability of autism rates for a significant number of years in the U.K. while breastfeeding rates were stable there (unlike in the U.S.), plus the progressively lower rates of autism among 2nd-, 3rd-, and 4th-born children (who have progressively lower exposures to toxins in breast milk).  And we have seen a key mechanism of social development (eye contact) proceed to derail after initial satisfactory postnatal development. The above all lead to important questions:

 

Q #1:  Given the presence of four different neuro-developmental toxins in typical breast milk, each of which typically far exceeds recognized safe levels and levels in infant formula, is there any reason why those exposures could not be a reasonable explanation for all of the unexpected outcomes mentioned?
 

Q #2:  Are there any toxins known to widely reach infants in doses well in excess of a recognized safe level (e.g., EPA’s RfD), aside from the four such toxins that are ingested by means of breast milk?  If so, please identify them.

 

 

The above Q #2 was mailed to seven members of the science team at the major autism-advocacy organization, Autism Speaks, and, as of several months later, of the three responses received, not one has offered an answer to that question.

 

The essential contents of the above Q #1 were mailed to the above scientists and also to the three U.S physicians’ associations that promote breastfeeding (the associations of pediatricians, obstetrician/gynecologists and family physicians) and the World Health Organization.  Of the three total responses received, not one has attempted to answer that question.

 

Those who promote breastfeeding or who even consider doing it ought to think carefully about the fact that nobody seems to be able to answer the above questions.

 

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

 

Another especially important reason to reconsider the type of infant feeding that is the focus of this article:  Something can be done to rapidly, greatly reduce infants’ exposures to this source of infant ingestion of toxins.  Recent major scientific studies have identified specific toxins that apparently lead to autism:  atmospheric pollution including diesel emissions27 (diesel emissions include dioxins, PCBs and PBDEs).  But few parents are able to move away from the locations that are high in this pollution; and a mother’s body burden of these “persistent” toxins is a result of many years of accumulation, so a move of residence would have only minor effect anyway, unless it is done years ahead of pregnancy.  And reduction of those pollutants in the environment and in the bodies of mothers is something that can only be worked towards, seeking reductions that could only come over a period of many years; but millions more children would be impaired for life in the meantime, while reductions of contaminants in breast milk come only gradually.  On the other hand, most parents could promptly discontinue the type of feeding that is channeling concentrations of developmental toxins to their infants at the most vulnerable stage of the infants’ lives.  All that is required is informing parents of what is presented here, to enable them to make informed decisions about breastfeeding.  At this point all that most parents know on the question of breast-vs.-bottle feeding is summarized in the catch-phrase as “breast is best.”

 

But isn’t breastfeeding recognized as beneficial for infants?   Of all the disorders that have been alleged by former U.S. Surgeon General Regina Benjamin to be reduced by breastfeeding, all but one has actually substantially increased in the U.S. since breastfeeding greatly increased, after 1971; in the case of that one disorder that did not increase, neither was it reduced following the major increases in breastfeeding.31   Although various studies have found beneficial effects to be associated with breastfeeding (always with known confounders present31a), over 60 scientific studies have found breastfeeding to be associated with worse health outcomes.32   As indication of the one-sidedness that prevails on this topic, if one goes to the websites of the American Academy of Pediatrics, the American Academy of Family Physicians, and the U.S. Department of Health and Human Services, and finds their presentations regarding breastfeeding, one can read numerous references to the studies that have found benefits of breastfeeding but no reference to any of the numerous studies that have found adverse effects of breastfeeding that apply to the general population.

 

So it is worth taking a closer look at the studies that have found benefits of breastfeeding.  Surgeon General Benjamin acknowledged that research on the health outcomes of different modes of infant feeding is limited to observational studies;”33 those are a study type that has been authoritatively determined to be of low quality.  One determination that evidence from observational studies is of low quality has been provided by Dr. Gordon Guyatt and an international team of 14 associates;34 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 refuted by high-quality studies.35  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),36  writing about “the disastrous inadequacy of lesser evidence,” in reference to findings from observational studies.37

 

 

For the U.S. generation born in the mid-20th century, breastfeeding was unusual.  That generation did not have the unexplained childhood epidemics and major increases that have become prevalent since then:  diabetes, asthma, allergies, obesity, ADHD and autism.  In the decades since 1971, there have been not only major increases but also lows and mid-levels of multiple childhood disorders that have correlated closely with preceding increases, lows and mid-levels of breastfeeding rates.(see www.breastfeedingprosandcons.info, www.autism-correlations.info, and www.child-disability.info, with many authoritative sources cited at all three websites.)  There are many other well-substantiated, authoritative reasons to doubt the popularly-accepted view about benefits of breastfeeding.32

 

Various U.S. doctors’ associations (American Academy of Pediatrics, American Academy of Family Physicians, American Congress of Obstetricians and Gynecologists) and WHO promote breastfeeding, but they appear to be unable to answer appropriate questions about the basis for their recommendations.  As mentioned, multiple letters to each of those organizations from the director of Pollution Action, asking how they have determined that the known toxins in breast milk are not having harmful effects, have never been responded to.  Medical authorities are promoting feeding infants a substance that is known to currently contain multiple developmental toxins, each of which is ingested in doses very far in excess of established safe levels, while several unexplained childhood epidemics and increases have arisen and are continuing; if those authorities who are doing the promoting are unwilling (or, more likely, unable) to answer questions about their recommendations, what does that say about the merits of their recommendations? 

 

 

Comments related to this are welcome, to be sent to:

 

*Donald P. Meulenberg, Director, Pollution Action, 33 McWhirt Loop, Ste. 115, Fredericksburg, VA 22406    

        or to  dm@pollutionaction.org       For information about Pollution Action, see  www.pollutionaction.org     

 

 

(A copy of this statement in PDF format is at www.breastfeeding-research.info/A.pdf

 

 

_______________________________

 For ease of referral to the sources indicated here, if there is no highlighted link, you can (a) use your cursor to drag on and select a URL from the footnote (select the letters beginning with www or http and ending just before the next space; be sure to select all of that but no more, not even a space), then (b) control - c  (to copy that); then (c) paste that (control - v) into the horizontal web-address slot at the top left of your browser page, then press ENTER on your keyboard. 

 

1)  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

1a)  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

 2)  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

 

 For ease of referral to the sources indicated here, if there is no highlighted link, you can (a) use your cursor to drag on and select a URL from the footnote (select the letters beginning with www or http and ending just before the next space; be sure to select all of that but no more, not even a space), then (b) control - c  (to copy that); then (c) paste that (control - v) into the horizontal web-address slot at the top left of your browser page, then press ENTER on your keyboard. 

2a)  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:

 

2b) 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

 

2c)  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)

 

 

3) "Surgeon General's Call to Action to Support Breastfeeding, 2011," p. 6 and Fig. 1,  at www.surgeongeneral.gov/library/calls/breastfeeding/calltoactiontosupportbreastfeeding.pdf

 

For ease of referral to the sources indicated here, if there is no highlighted link, you can (a) use your cursor to drag on and select a URL from the footnote (select the letters beginning with www or http and ending just before the next space; be sure to select all of that but no more, not even a space), then (b) control - c  (to copy that); then (c) paste that (control - v) into the horizontal web-address slot at the top left of your browser page, then press ENTER on your keyboard. 

 

 

3a) 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)

 

 

3b)  Jensen, A.A. et al, Chemical Contaminants in Human Milk, CRC Press, Inc., Boca Raton, Ann Arbor, Boston, 1991, p 15.  This is fully compatible with the statement by two other experts as follows:  “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.” (Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. Lancet. 2006;368:2167–2178

at www.reach-compliance.eu/english/documents/studies/neurotoxity/PGrandjean-PjLandrigan.pdf p. 2  Other earlier research that is still cited decades later is compatible with this: Gallenberg et al., Transfer of persistent chemicals in milk. Drug Metab. Rev. 1989;21:277-317

This is also compatible with the very large differences between concentrations of toxins in breast milk and those in alternative infant feeding -- see Section 2, cont. 

Also see Needham et al., Partition of Environmental Chemicals between Maternal and Fetal Blood and Tissues, Environ Sci Technol. Feb 1, 2011; 45(3): 1121–1126,  at  http://pubs.acs.org/doi/pdf/10.1021/es1019614, Table 2, finding weight-based concentrations of organohalagens to be over 30 times higher in human milk than in umbilical cord tissue.

3c)  U.S. ATSDR document on PCBs, Section 3.7, pp. 391, 381, at http://www.atsdr.cdc.gov/ToxProfiles/tp17.pdf

 

4) Taylor et al., Prevalence and incidence rates of autism in the UK: time trend from 2004–2010 in children aged 8 years.  BMJ Open  2013;3:e003219. doi:10.1136/bmjopen-2013-003219 at http://bmjopen.bmj.com/content/3/10/e003219.full.pdf+html?sid=01d45cb4-5ed1-45fd-91fe-c1544700b513

5) catalogue.ic.nhs.uk/publications/public-health/surveys/infant-feed-surv-2010/ifs-uk-2010-sum.pdf , Ch. 2, p.13

6) CDC’s 2011 Pediatric Nutrition Surveillance, National Summary of Trends in Breastfeeding, Table 13D, at www.cdc.gov/pednss/pednss_tables/pdf/national_table13.pdf

7) Schecter A et al., Polybrominated diphenyl ethers (PBDEs) in U.S. mothers' milk.  Environ Health Perspect. 2003 Nov;111(14):1723-9 www.ncbi.nlm.nih.gov/pubmed/14594622

 

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8) -- Durkin et al., Advanced Parental Age and the Risk of Autism Spectrum Disorder, Am J Epidemiol. 2008 December 1; 168(11)  Table 3’s “Birth order” section, at  www.ncbi.nlm.nih.gov/pmc/articles/PMC2638544; this study was referred to in 2009 as the largest of its kind  (in “US researchers find link between age, birth order and autism,” theguardian.com, 7 January 2009); it studied a birth cohort of over 250,000.

 -- Croen et al., Maternal and Paternal Age and Risk of Autism Spectrum Disorders, JAMA Pediatrics, April 2007, Vol 161, No. 4  http://archpedi.jamanetwork.com/article.aspx?articleid=570033#poa60107t3 

 -- Durkin (2008) also referred to another study supporting correlation of increased autism with earlier birth order: Glasson et al. Perinatal factors and the development of autism. Arch Gen Psychiatry. 2004;61(6):618–627.

 

9a)  Ryan et al., Program for Women, Infants, and Children Participants, 1978 -2003: Lower Breastfeeding Rates Persist … in journal Pediatrics, at http://pediatrics.aappublications.org/content/117/4/1136.full.pdf+html , Table 2, “Parity” section.

 

9b) -- CDC chart at www.cdc.gov/breastfeeding/data/NIS_data/2006/socio-demographic.htm

 

9c) -- PCDDs, PCDFs, and PCBs concentrations in breast milk from two areas in Korea: body burden of mothers and implications for feeding infants,  Jiyeon Yang et al. Chemosphere 46 (2002) 419–428); and   Infant Exposure to Chemicals in Breast Milk in the United States: Judy S. LaKind, et al.,  Children's Health Review Environmental Health Perspectives • Volume 109 | Number 1 | January 2001  www.ncbi.nlm.nih.gov/pmc/articles/PMC1242055/pdf/ehp0109-000075.pdf

 

10) Rice et al., Critical Periods of Vulnerability for the Developing Nervous System:  Evidence from Humans and Animal Models, EPA National Center for Environmental Assessment, at www.ncbi.nlm.nih.gov/pmc/articles/PMC1637807

11) Rodier, “Developing Brain as a Target of Toxicity,” Environmental Health Perspectives, at www.ncbi.nlm.nih.gov/pmc/articles/PMC1518932/pdf/envhper00365-0077.pdf

11a) Pesticides in the Diets of Infants and Children, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C.  1993, p. 60

 

12) Sec. 4 of Gadad et al., Neuropathology and Animal Models of Autism: Genetic and Environmental Factors,  Autism Res Treat. 2013: 731935 PMCID: PMC3787615 at www.ncbi.nlm.nih.gov/pmc/articles/PMC3787615

13) Dobbing et al., Quantitative growth and development of human brain, Arch Dis Child, 1973 October: 48(10): 757-767 at www.ncbi.nlm.nih.gov/pmc/articles/PMC1648530)  80% figure estimated from Figure 11.

14) Sokolowski et al., Methylmercury elicits mitochondrial-dependent apoptosis in developing hippocampus and acts at low exposures, Neurotoxicology  2011 at www.ncbi.nlm.nih.gov/pmc/articles/PMC3256128

 

 For ease of referral to the sources indicated here, if there is no highlighted link, you can (a) use your cursor to drag over and select a URL from the footnote (select the letters beginning with www or http and ending just before the next space; be sure to select all of that but no more, not even a space), then (b) control - c  (to copy that); then (c) paste that (control - v) into the horizontal web-address slot at the top left of your browser page, then press ENTER on your keyboard. 

 

15) Chien LC, et al., Analysis of the health risk of exposure to breast milk mercury in infants in Taiwan. Chemosphere. 2006 Jun;64(1):79-85. Epub 2006 Jan 25 at http://www.ncbi.nlm.nih.gov/pubmed/16442149  Note that “mercury” and “methylmercury” are often used interchangeably, including by the EPA (see www.epa.gov/hg/effects.htm), since it is typically difficult to differentiate the various species of mercury.  It is recognized that a high percentage of the mercury in human bodies is methylmercury.  According to the U.S. Geological Survey, methylmercury is “the form of mercury that is most easily bioaccumulated in organisms;” and it “biomagnifies (increases in concentration as it travels up the food chain)."  Bear in mind that humans are at the top of the food chain, especially with regard to eating of fish and seafood in the case of methylmercury.

16) Jones et al., Attention to eyes is present but in decline in 2-6-month-old infants later diagnosed with autism: Nature:(2013) DOI:doi:10.1038/nature  at www.pediatrics.emory.edu/documents/divisions/autism/Jones_Klin_2013.pdf

17) Abraham et al., POP accumulation in infants during breast-feeding. Organohalogen

Compounds 48:25–26 (2000), as reported in Infant Exposure to Dioxin-like Compounds in Breast Milk,  Lorber et al., Vol.110 | No. 6 | June 2002 • Environmental Health Perspectives  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240886/pdf/ehp0110-a00325.pdf

 18) P. Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants,  Environ. Health Perspectives, accepted Oct. 1993   www.ncbi.nlm.nih.gov/pmc/articles/PMC1567218/pdf   Also  Marques RC, et al., Hair mercury in breast-fed infants exposed to thimerosal-preserved vaccines. Eur J Pediatr. 2007 Sep;166(9):935-41. Epub 2007 Jan 20  at www.ncbi.nlm.nih.gov/pubmed/17237965   (Re: especially rapid mercury transmission in early postnatal weeks): Exploration Of Perinatal Pharmacokinetic Issues  Contract No. 68-C-99-238, Task Order No. 13  Prepared for EPA by:  Versar, Inc.  EPA/630/R-01/004   Section 4.7.4.3,  at www.epa.gov/raf/publications/pdfs/PPKFINAL.PDF

 

18a) Burbacher et al., Comparison of Blood and Brain Mercury Levels in Infant Monkeys Exposed to Methylmercury or Vaccines w/ Thimerosal, Environ Health Perspect. PMC1280342  at   www.ncbi.nlm.nih.gov/pmc/articles/PMC1280342

19)  "Breastfeeding, Family Physicians Supporting (Position Paper)," American Academy of Family Physicians at  www.aafp.org/about/policies/all/breastfeeding-support.html

20)  Environmental Health Perspectives (of NIH), Vol. 109, No. 1, Jan. 2001, Fig. 3 at www.ncbi.nlm.nih.gov/pmc/articles/PMC1242055/pdf/ehp0109-000075.pdf

21) U.S. Geological Survey web page on mercury at www.usgs.gov/themes/factsheet/146-00 Laks DR, .Assessment of chronic mercury exposure within the U.S. population, National Health and Nutrition Examination Survey, 1999–2006 . Biometals. 2009 Dec   at www.ncbi.nlm.nih.gov/pubmed/19697139

 

 For ease of referral to the sources indicated here, if there is no highlighted link, you can (a) use your cursor to drag over and select a URL from the footnote (select the letters beginning with www or http and ending just before the next space; be sure to select all of that but no more, not even a space), then (b) control - c  (to copy that); then (c) paste that (control - v) into the horizontal web-address slot at the top left of your browser page, then press ENTER on your keyboard. 

 

 

 22) Sec. II.B of Brominated Flame Retardants, Third annual report to the Maine Legislature, 2007, D Rice et al. www.maine.gov/dep/waste/publications/legislativereports/documents/finalrptjan07.pdf, citing Li et al., 2005a

23) Table 3 of Developmental Neurotoxicity of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Costa et al., Neurotoxicology. 2007 November; 28(6):   NIHMS34875 at  www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052  

24) Gascon M et al., Effects of pre and postnatal exposure to low levels of polybromodiphenyl ethers on neurodevelopment and thyroid hormone levels at 4 years of  age. [Environ Int. 2011]  . at www.ncbi.nlm.nih.gov/pubmed/21237513

24a)  Geier DA et al., Blood mercury levels in autism spectrum disorder: Is there a threshold level?  Acta Neurobiol Exp (Wars). 2010;70(2):177-86, www.ncbi.nlm.nih.gov/pubmed/20628441.  Also see footnotes 6, 15, 16, and 29  in D. Austin, An epidemiological analysis of the ‘autism as mercury poisoning’ hypothesis’, International Journal of Risk and Safety in Medicine, 20 (2008) 135-142  at  http://researchbank.swinburne.edu.au/vital/access/manager/Repository/swin:9302

24b)  Re: PBDE levels in breastfed vs formula-fed children:   Near end of Section 5.6.2 ("Impacts to Infants from Consumption of Breast Milk"), p. 5-79, of An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. online at http://www.epa.gov/ncea  or directly at  http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404   The above is compatible with authoritative reports of breast milk concentrations of PBDEs (a persistent developmental toxin) being over 30 times those in infant formula:  Schecter et al., Polybrominated Diphenyl Ether (PBDE) Levels in an Expanded Market Basket Survey of U.S. Food and Estimated PBDE Dietary Intake by Age and Sex, Environ Health Perspect. Oct 2006; 114(10): 1515–1520  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1626425   and also

 PBDEs in infant formula: Section 4.7 , p. 4-77, 2nd paragraph (citing Schechter et al.) of U.S. EPA (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment; EPA/600/R-08/086F. online at www.epa.gov/ncea or directly at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404

 

 25)  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 

 

26)  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

 

26a) 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 

 

26b) 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).

 

 

For ease of referral to the sources indicated here, if there is no highlighted link, you can (a) use your cursor to drag over and select a URL from the footnote (select the letters beginning with www or http and ending just before the next space; be sure to select all of that but no more, not even a space), then (b) control - c  (to copy that); then (c) paste that (control - v) into the horizontal web-address slot at the top left of your browser page, then press ENTER on your keyboard. 

 

27)  Roberts et al., "Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ Health Study II Participants," (Environ Health Perspect; DOI:10.1289/ehp.1206187 online at http://ehp.niehs.nih.gov/1206187)

-- Volk et al., Traffic Related Air Pollution, Particulate Matter, and Autism, JAMA Psychiatry. Jan 2013; 70(1): 71–77.   at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019010/

doi:  10.1001/jamapsychiatry.2013.266

 

 28) Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. Lancet. 2006;368:2167–2178. at www.reach-compliance.eu/english/documents/studies/neurotoxity/PGrandjean-PjLandrigan.pdf  p. 2

 31) see www.breastfeedingprosandcons.info and www.autism-correlations.info, with many authoritative sources cited at both websites.

 31a) see www.breastfeeding-benefits.net for considerable detail on this topic.

 32) see www.breastfeeding-studies.info

 33) p. 33 in the Surgeon General’s Call to Action to Support Breastfeeding, 2011 at http://www.surgeongeneral.gov/library/calls/breastfeeding/calltoactiontosupportbreastfeeding.pdf

34) Figure 2 in Guyatt et al., GRADE guidelines:  1. Introduction -- GRADE evidence profiles and summary of findings tables, Journal of Clinical Epidemiology, at http://www.jclinepi.com/article/S0895-4356(10)00330-6/pdf

35) Dr. Gordon Guyatt is chief editor of User’s Guides to the Medical Literature:  A Manual for Evidence-based Clinical Practice, 2nd Edition (3rd is upcoming), copyright  American Medical Association, published by McGraw Hill.

36) Writing in The Canadian Medical Association Journal, as quoted in “Do We Really Know What Makes Us Healthy?” New York Times, published: September 16, 2007  at http://www.nytimes.com/2007/09/16/magazine/16epidemiology-t.html?pagewanted=2&_r=0

37) In a review in the Journal of the Medical Library Association, only two guides are recommended for use by physicians in evaluating evidence in medical literature, one of which is the one edited by Guyatt et al., already referred to, and the other of which is by Dr. Sackett. (Journal of the Medical Library Association, Oct. 2002, User’s Guide to the Medical Literature:  A Manual for Evidence-Based Clinical Practice, Review by Rebecca Graves, at httpi://www.ncbi.nlm.nih.gov/pmc/articles/PMC128970)

 

 

 

 

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