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

 

 

Recent Research related to Autism, and

Connections with Environmental Toxins in Breast Milk

 

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 three neuro-developmental toxins 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 three times but up to 40 times the EPA’s RfD;2a  and

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

 

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  All three of the above are present in infant formula in concentrations less than 2% as high, and usually less than 1% as high, as their concentrations in human milk.3a

 

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 unexpected relationship involving autism:  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 from first to later children.8  Infants later in birth order  (a) are less likely to be breastfed, (b) are breastfed for shorter periods on average, 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.9

 

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

 

http://www.autism-research.net/image002.gifBreast milk (with its undisputed content of at least three 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 development takes place during the first year after birth.(see chart and footnote10)     According to EPA researchers, an organ is generally at its greatest vulnerability to environmental toxicants if exposure to the toxins occurs during development of that organ.11

 

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.

 

The cerebellum and autism

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.

 

………………………

 

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

………………………

 

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 average 3 times but go up to 40 times the EPA’s RfD, and also that concentrations of PBDEs in infant formula have been found to be less than 2% as high as in human milk.

   3) 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 of the above three chemical exposures would be highly significant when considering toxic effects on infants that occur shortly after birth, and which could therefore help explain the postnatal derailment.  But consider that all three exposures are regularly taking place, via breast milk, within the same child. 

 

Also 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; (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  (d) mercury, emitted by fossil fuel combustion, has increased several-fold in the environment of modern generations;21 (e) a study of sediment from multiple locations in the Great Lakes found an increase of PBDE levels by a factor of several hundred times since the 1970s.22   PBDE concentrations in human milk in Canada were found to increase 7-fold between 1992 and 2002.23  

 

 

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, (b) measured mercury levels in children far past the vulnerable early-postnatal period, or (c) assessed effects at too young an age to properly judge the long-term results.)  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.)

 

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 been postnatal, 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 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 extremely high levels of toxins are continuously ingested by a breastfed infant during the period when the brain is especially vulnerable to toxins due to its rapid growth (see above chart, and for more information see www.autism-research.net/postnatal-effects.htm). 

 

Related to the above:  A highly-published scientist and Fellow of the American College of Nutrition found, on the basis of data from all 50 states and 51 U.S. counties, 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."25    Another U.S. study and a U.K. study arrived at similar findings.26

 

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

 

…………………………

 

So we have the unexpected close geographic correlations of autism with breastfeeding, 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 surprisingly low rate of autism among later-born children (who have far lower exposure to toxins in breast milk than earlier-born children).  And we have seen a key mechanism of social development (eye contact) proceed to decline after initial postnatal normalcy. The above all lead to important questions:

 

Q #1:  Given the presence of three 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 toxins that are ingested by means of breast milk?  If so, which ones are those?

 

 

Considerable research has gone into infant exposures to developmental toxins over many years, so this is a reasonable time to take stock and to try to see what has been learned.  If several toxins have been found to reach infants in known hazardous quantities via a single means of ingestion, and if no toxins have been found to reach infants in such doses by any other means, doesn’t that mean we should seriously consider doing something about the specifically-identified means of ingestion of hazardous levels of toxins?

 

Remember that exposure of infants to important toxins that accumulate in breast milk results in “infant exposure that exceeds the mother’s own exposure by 100-fold on the basis of bodyweight.”28   Also remember that, of the three sources of infant mercury exposure, breast milk, inhalation, and dermal exposure, breast milk was found to provide 96 to 99.6% of the total exposure.11  Combine the above with awareness that the infant brain’s greatest vulnerability to toxins appears to be high in the year after birth (see earlier chart and accompanying text).  Then consider how likely it is that any toxin could be of sufficient impact on infants during the period of rapid brain development as to cause these disorders unless it reached infants via the concentrating process of lactation.

 

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.  For considerable information on this topic, go to www.autism-researh.info/postnatal-effects.htm

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

 

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.  Specific toxins that apparently lead to autism have been identified:  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 the 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.  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 are said by the U.S. Surgeon General 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 desirable effects to be associated with breastfeeding (always with known confounders present), over 50 scientific studies have found breastfeeding to be associated with worse health outcomes,32   Among those was the study that was apparently the only study on effects of breastfeeding on childhood obesity that was randomized, which is the recognized best way to avoid effects of the confounders that often cause false conclusions in typical studies. 

 

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.31  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.  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? 

 

For additional relevant information, see www.breastfeeding-toxins.info and  www.breastfeeding-and-autism.net.

 

There is a widespread notion that prenatal exposures to toxins, rather than postnatal, are the only significant harmful exposures for developing nervous systems.  But there is also a tremendous amount of information from authoritative sources and from dozens of scientific studies to correct that misconception.  See www.breastfeeding-research.info/postnatal-effects.htm

 

It is often said that human milk contains immune cells that help ward off infections in the breastfed child.  This is not disputed, but there is an extremely serious question as to whether that short-term benefit stunts the development of the child’s own immune system, resulting in long-term harm.  There have been epidemics in childhood and young-adult immune-related diseases that have arisen since breastfeeding went from unusual to widespread, after 1971. To read about the “hygiene hypothesis” in this regard, go to www.breastfeeding-research.info/hygiene-hypothesis.htm, and to read about increases in childhood diseases after 1971, go to www.breastfeedingprosandcons.info. 

 

It is well established that risk of autism is much higher in children of older mothers than in children of younger mothers.  The reasons for that are currently being researched, but the fact that older mothers are known to have far higher body burdens of “persistent bioaccumulative toxins” than younger mothers seems to be a logical explanation; this is especially true since some of those toxins are transmitted to breastfed infants in concentrations recognized to be far above established relatively safe levels.  For details, see www.autism-research.net/older-mother-autism-risk.htm.

 

Research published in 2014 has found “patches of disorganization” in brains of children with autism (examined postmortem), and there is an opinion that this disorganization has its origins in prenatal development.  But there are excellent reasons to see that the observed disorganization actually originates postnatally, due to postnatal exposures to developmental toxins.   For details, see www.autism-research.net/brain-impairment.htm.

 

 

 

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

 

*Donald P. Meulenberg, Director, Pollution Action,

at  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

 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 of 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:  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 study in first page of table.   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:

- EPA Technical Fact Sheet on Polybrominitated Diphenyl Eithers (PBDEs) and PBBs, p.3   at  www.epa.gov/fedfac/pdf/technical_fact_sheet_pbde_pbb.pdf   Regarding prevalence of tetraBDEs, see 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.

2b) Re:  Mercury levels in breast milk:

- U.S. ATSDR document on mercury at www.atsdr.cdc.gov/toxprofiles/tp46-c5.pdf, p. 443

- Code of Federal Regulations, Title 21, Chapter 1, Subchapter B, Part 165, Subpart B, Sec. 165-110 at  http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfCFR/CFRSearch.cfm?fr=165.110

 

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

 

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

 

 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. 

 

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.

 

9) -- 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.

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

 -- Factors Influencing Full Breastfeeding in a Southwestern Ontario Community: Assessments at 1 Week and at 6 Months Postpartum  Tammy J. Clifford, PhD  Human Lactation, 2012  at http://jhl.sagepub.com/content/22/3/292.abstract

 -- PCDDs, PCDFs, and PCBs concentrations in breast milk from two areas in Korea: body burden of mothers and implications for feeding infants, Yang et al., Chemosphere 46 (2002)    and Infant Exposure to Chemicals in Breast Milk in the United States, LaKind et al., Children’s Health Review  Environmental Health Perspectives  Vol 109 Jan 2001  www.ncbi.nlm.nih.gov/pmc/articles/PNC1242055/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

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) Infant Exposure to Dioxin-like Compounds in Breast Milk  Lorber et al., Vol.110 | No. 6 | June 2002 • Environmental Health Perspectives  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) For details, see Appendix 2a at http://www.pollutionaction.org/breastfeeding-and-autism-and-cancer.htm

 

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): 

 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.

 32) see www.breastfeeding-studies.info

 

 

 

 

 

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