(DRAFT) Autism and Mental Impairment: Breastfeeding as a Contributing Cause to the Increase in Male Impairment, and other Factors Contributing to the Major Decline in Female Mental Impairment
by Donald P. Meulenberg
Summary:
The male-to-female ratio of mental impairment among people born in the U.S. during the last two decades has become two-to-one, which appears to be a recent development. It contrasts sharply with the even ratio that apparently prevailed among those born in the half-century leading up to the mid-1970's. In the intervening years, there was a transition in the male-female ratio, with an intermediate degree of unevenness. (Data drawn from U.S. Census Bureau website, which based data on questions concerning residents' possible "serious difficulty concentrating, remembering, or making decisions"; see endnote (1).)
One side of the above transition is due a major decline in the mental impairment rate among 5-to-17-year-old girls; the rate dropped to only 2.6% of those born since the early 1990's, compared with the 4.6% rate that represents the generations born in the three decades leading up to the mid-'70's. The rest of the change has come from a major increase in the rate of reported mental impairment among 5-to-17-year-old boys, climbing to an average rate of 5.2%. Census Bureau data indicate serious mental difficulties for about one out of eleven boys in Maine and about one out of twelve in Rhode Island, even without considering the probably greater prevalence of impairment among those born more recently.
A disorder that is closely related to this discussion is autism (or ASD, Autism Spectrum Disorder), which includes a high percentage of mentally impaired among those affected by the spectrum of symptoms. ASD is especially of interest with regard to the general growth in mental impairment among males, since (a) autism, also, has been growing during this same period, and (b) autism, also, affects far more males than females.
As background to the major changes that have apparently taken place in mental impairment rates, it should be pointed out that there was an approximately 90% decline that took place in environmental lead over recent decades, beginning in the 1970's, and also a major decline in releases from major sources of dioxins, including dioxin-related PCBs. These substances are known to be neurological toxins, affecting infants and/or fetuses especially. So a decline in mental problems should have been expected, and in fact there was a major decline among females. What should be demanding our close attention is the large increase in mental disability among males that took place during that same period, when there were excellent reasons to expect instead a large decrease.
The hormone that is produced by the male testicles, testosterone, is known to be critical to development of the infant brain. There are certain neurological toxins that have been increasing substantially in the environment in recent decades that are known to cause testicular atrophy or to harm mental development of males specifically: DEHP, PBDEs, certain pesticides, and certain dioxins (some forms of dioxins have been decreasing, but others that closely affect humans have been increasing rapidly). Apparently those chemicals reach the developing fetus and infant principally as a result of their long-term build-up in the body of the future mother. They can then affect the development of the fetus during gestation and can also, more importantly, affect the developing infant via breast milk in which the toxins are excreted.
Much evidence is presented in this paper regarding certain neuro-developmental toxins in the environment and how they affect developing infants, especially toxins that affect male infants specifically. These toxins are known to accumulate in the body and later be excreted in breast milk; there is no disagreement that the toxins are ingested in far greater quantities by breastfed infants than by formula-fed infants or by adults. As mentioned, several of these toxins have been rapidly increasing in the environment during the same period during which mental impairment among recently-born males has been increasing. Greatly adding to the problem is that breastfeeding has been becoming more widespread during the same period.
Organizations and government agencies that promote breastfeeding do so partly on grounds that breastfed children have fewer of various illnesses than formula-fed children. Their position, based on studies, is that there are health benefits of breastfeeding; and they feel that those benefits outweigh the possible harm caused by the toxins in breast milk. The view of the present author is that a general advocacy of breastfeeding does not pay sufficient attention to what is now known about hazards of toxins known to be present in typical present-day breast milk in the more populated sections of at least some industrialized countries, including the U.S.
Epidemiological evidence will be presented in this paper showing the following:
a) very strong correlations between high rates of autism and higher rates of breastfeeding in various countries, U.S. states, and ethnicities; a roughly 50% lower rate of breastfeeding among U.S. blacks than among whites, corresponding with a roughly 50% lower rate of autism among blacks, is only one of many associations;
b) unusually low rates of autism in every one of the seven U.S. states in which breastfeeding has been found to be relatively rare.
c) very good life expectancies in countries with low rates of breastfeeding, comparing so well with life expectancies in countries with higher levels of breastfeeding that there is excellent reason to believe that, at minimum, there are no overall long-term unfavorable physical health consequences of greatly reduced breastfeeding.
d) in the cases in which high rates of breastfeeding don't correlate with high levels of autism, there always appears to be good reason to believe that the average breast milk in that area is relatively low in levels of developmental toxins.
Also of likely interest to many parents is the fact that some chemicals typically present in breast milk are known to cause de-masculinization of male test animals and (in some cases) masculinization of female animals. The three Western European countries that stand out with the highest levels of breastfeeding (all Scandinavian) are all so exceptionally protective of gay rights that one could reasonably suspect a causal connection between culturally-high levels of breastfeeding and unusually high percentages of gay citizens in those countries. There is one U.S. major city that, based on the Scandinavian ethnicity of the state's residents, could be predicted to have the highest rate of breastfeeding of any city in the U.S. (Minneapolis); in what might be more than pure coincidence, fairly thorough research has found Minneapolis to be the "Gayest City" in the U.S.
There are other probable avenues by which infants can ingest or absorb environmental toxins that could result in abnormal mental developments, such as ingestion of soil that is not suspected of being contaminated, ingestion of typical dust, and absorption through the skin or breathing of widely-occurring, recently-prevalent toxins that can interfere with activity of male testosterone, which is known to be important to neurological development. Some of these other probable sources of neurological deviations are also dealt with in this paper.
The following should be pointed out regarding the seriousness of some of the problems being discussed here: Over 5% of recently-born American males being reported as having mental difficulties, and that proportion apparently growing rapidly at a time when such disability should have been expected to be declining (and was declining for females), speaks for itself. According to the CDC, over 35,000 children are born in the U.S. every year who will probably eventually be diagnosed with Autism Spectrum Disorder alone, and those are far from all of the recently-increased percentage of males with mental impairment. Estimates of the average total lifetime cost of caring for a mentally-impaired person with ASD have varied between $3.2 million and $4.7 million.(1b)
Attention should also be paid to the apparent major decline in mental impairment that has taken place among female children. This is a recent development, one which this author has found mentioned almost nowhere outside the bare statistics in the many data tables in the website of the U.S. Census Bureau. As indicated above, that decline in female mental impairment coincides closely with major declines in certain known developmental toxins in the environment, and a causal relationship is very likely. This appears to be a tremendous success story for the regulatory efforts that resulted in those declines, a result from which we should learn as much as possible, so that we can best achieve even greater benefits from further, similar efforts.
Some lessons to be learned: (a) successful past regulatory efforts should be extended and increased whenever possible, including by removing the exemption that still allows aviation fuel to contain lead; (b) <<??>> regulators should recognize that cooperation from a concerned citizenry is important, therefore they should not allow political correctness to prevent them from using terms that convey the true seriousness of the consequences of exposure to toxins (such as by using "developmental delay" to describe what is normally a permanent, life-impairing condition); (c) it should be recognized how very powerfully certain common environmental toxins are related to neurological development, and how different toxins can affect the two genders differently. Some influential people believe that environmental pollutants are not causing mental impairment in a substantial way, and their influence is helping prevent action and additional research that could have considerable benefit in preventing future mental impairments. If anybody is heard alleging that mental impairment (including autism) is not closely associated with environmental toxins, that person should be asked to provide an explanation as to why mental impairment among recently-born females has declined so substantially in recent decades. Heredity could not possibly account for such a rapid decline.
It must be acknowledged that a great many theories have been advanced as to environmental causes of autism, most or all of which have been found not to be well substantiated by evidence. Recognizing that, and with excellent grounds to believe that his evidence is very strong, the author of this paper encourages anybody to try to provide rebuttals to any points presented here. All comments received will be respectfully received, responded to, and included in a section at the end of this paper. Please send comments to dm@pollutionaction.org
Proposed Remedial Actions: For parents-to-be who can plan ahead, the ideal action would be for the woman (years before pregnancy) to adopt a diet that mainly avoids the meat, dairy products and fish that are the main sources of dioxins and mercury into her body, so that she could feed her future infant good-quality breast milk, and also minimize effects of toxins during gestation. If it is too late for that, she should become aware of the risks of breastfeeding as presented in this paper, and act accordingly. Other ways to protect future nursing mothers and developing infants from neurological toxins include keeping them away from known sources of toxins (including near well-travelled highways, railroad tracks and airports, and downwind from wildfires), aggressive publicity discouraging eating by infants of foods known to contain high levels of dioxins and/or mercury (especially ground beef and foods high in fat), thorough air filtration and frequent removal of dust (especially in areas where infants could be kept most of the time during critical stages of their brains' developments), refraining from enclosing the infant male scrotum in (possibly dioxin-contaminated) bleached disposable diapers, separation of infants from tobacco smoke, and minimizing exposure of infants to possible ingestion or absorption of DEHPs contained in soft plastics. Practicality of unusually good air filtration during periods of bad air could be improved by focusing more research on "critical windows of sensitivity" during which the developing brain has been found by scientific research to be especially vulnerable to effects of toxins. Many more suggestions for remedial actions will be presented near the end of this paper.
Acknowledgement of this author's personal bias, of a kind that many people object to: I believe that, where there is reasonable doubt about the safety of a substance to which people are exposed in the environment, the benefit of the doubt should be on the side of trying to minimize human exposure to that substance. In presenting my concerns to various people, some have pointed out that there isn't solid proof that the substances in question cause the harm that I am concerned about. They are likely to recommend that high standards of evidence should first be met (involving research that could take place only over many years, requiring funding, personnel and/or equipment that may or may not be available) before attempts should be made to discourage a usage or activity that is seriously in question. In line with that kind of orientation, at least two pesticides, endosulfan and dicofol, had been in use in the U.S. since the 1950's before a study by researchers with the state of California found autism to be several times higher than average among infants residing in areas where it was used. Not long after that, following almost a half-century of widespread use, the EPA discontinued the registration for those pesticides. And bear in mind that the association between smoking and lung cancer was suspected for decades before evidence was finally provided that conclusively proved the connection. Also note that discovering the toxicity of Thalidomide was greatly aided by the facts that it was a new drug and that its effects were completely obvious at birth, and relatively frequent, and caused by one particular toxin; it is much more difficult to conclusively zero in on the various toxins probably contributing to the spectrum of autism disorders, which toxins are merely increasing in the environment and in breast milk. My hope is that people will read this paper who believe in paying serious attention and minimizing risk even when there are only good grounds for suspicion about a substance or practice, and who see some validity to what is referred to as the "precautionary principle."
Note from and about the author, and other acknowledgements: There can be advantages to having a study done by a qualified outsider. Research by PhD's tends to go into great detail in narrowly-defined areas, and they typically conclude with recommendations for future multi-year studies on the subject under consideration. I feel that this matter deserves a strong orientation toward determining what can and should be done now to address the problem. I've found that there is already a large amount of knowledge published that relates to this subject, which can be brought together, analyzed and put promptly to use. I received scores in the top 1% on standardized tests when in high school, hold an A.B. cum laude from Oberlin College, did well in challenging biology and chemistry courses, and stood in the top third of my class during a year at Harvard's Graduate School of Business Administration. There were important aspects of the business-school case-study method that have been helpful in making this paper more practically useful (I believe) than much or most of what has been written on the subject, as follows: After carefully studying large amounts of printed matter available on a subject, one is expected to come up with well-considered recommendations for action. Apparent insufficiency of information available on a subject should not lead one to be satisfied to recommend future long-term studies, if there is a serious problem now. Work around gaps in the available data as best you can, and come up with an action plan reasonably quickly that you can defend in plain English on the basis of the data and common sense. As applied in this case, that approach meant poring through hundreds of studies and reports, plotting local disability data and analyzing regional pollution data sets (with the aid of spreadsheet software), winnowing out some apparent patterns, utilizing the excellent computer expertise, diligent data analysis and real-world knowledge of Matt Hulbert, data entry and map-shading assistance from various helpers, considerable assistance from reference librarians at the Central Rappahannock Regional Library in locating difficult-to-access scientific articles, very helpful thoughts and guidance to information sources from Professor James Corbett of the University of Delaware's College of Earth, Ocean, and Environment, and drawing on insightful comments and suggestions from various acquaintances, employees and friends, including parents from three separate families each with at least one boy and one girl. Normal business calculations are lacking here, for good reason; the costs of most of my proposed remedial measures are so minimal in relation to the lifetime costs of mental impairment that calculations are unnecessary; most would also protect the infant and other family members against exposure to known or probable carcinogens, some would probably also improve immune function (Gehrs BC, Riddle MM, Williams WC, Smialowicz RJ (1997). "Alterations in the developing immune system of the F344 rat after perinatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin: II. Effects on the pup and the adult." Toxicology 122(3):229-40) , and several would actually save money (such as stopping smoking and eating less meat). Other preventive steps that parents are advised to consider are ones the cost of which only they could calculate, including possibly re-locating to areas where pollution levels are lower while they have infants developing. In any case, we should not have to wait for completion of ongoing five-year studies before taking constructive steps.
Full disclosure/ verifiability: I own a small U.S. manufacturing company that competes in a minor but significant way with imports from Asia. My attention was drawn to the subject of mental impairment partly by seeing an increase in sales of our damage-resistant products for use in residences for mentally-disabled young people, but also by awareness of the increasing toxic pollution emitted by ships bringing imports to U.S. shores. That pollution is presented in this paper as one source (but only one of many sources) of atmospheric toxins that are probably involved in causing mental impairment. I have tried to include the authoritative governmental and professional source(s) for every statement of importance in this paper that doesn't seem to be common knowledge, unless it is something original based on stated reasoning that I believe most people would consider valid. Anyone with internet access can check the sources on which this paper was based, in the websites whose addresses are indicated. Where non-everyday-software is needed for viewing the original data sources, it is almost always widely-available software; and guidance is typically provided (in footnotes) on accessing the data when it isn't obvious how to do so. I strongly encourage any reader to look in this paper for any statement that does not appear to be well supported by valid evidence or reasoning, or any passages that don't seem to make sense, and to inform me (and anyone else) about any apparent flaws. My e-mail address is dm@pollutionaction.org .
Part I: Some Specific Probable Environmental Causes of Neurological Impairment
1.1 A preview, with much more to follow:
Figure 1


1.2.a PAHs and Dioxins, acting as Mutagens or Endocrine Disruptors
Dioxins and certain PAHs (Polycyclic Aromatic Hydrocarbons) are categories of chemicals widely distributed in the environment that are implicated as sources of neurological impairment. The specific means by which they cause harm is by acting as "endocrine disruptors" (in the cases of dioxins and at least one PAH) or as mutagens (in the case of some PAHs). A web page of the National Institutes of Health says that endocrine disruptors are "chemicals that may interfere with the body’s endocrine system and produce adverse developmental, reproductive, neurological, and immune effects in both humans and wildlife. …. ." (emphasis added) The determination of dioxins and dioxin-like substances as being endocrine disruptors is well established. At least one PAH appears to be clearly in the category of endocrine disruptors (see Figure13a2); screening of other chemicals for endocrine disruption properties is a very incomplete, ongoing process.* *(*It was only in late 2009 that the EPA issued its test orders for an "initial list" of chemicals to be screened as possible endocrine disruptors; screening of that initial list of chemicals is "underway" as of October, 2011. (at http://www.epa.gov/oscpmont/oscpendo/ ) ) In addition, other PAHs have been identified as mutagens, which can have adverse effects on the ways organs including the brain develop.
The EPA's web pages and documents on dioxins and PAHs point out major sources of dioxins and PAHs, as follows:
(a) dioxins are unintentional byproducts of several industrial chemical processes and of most forms of combustion, including fuel emissions, forest fires, and waste combustion, and are also found in weed killers used on agricultural lands;
(b) PAH's are also unintentional products of typical forms of combustion, including cigarette smoking and residential wood burning.
Quoting from the NIH's web page on endocrine disruptors, "Endocrine disruptors …may mimic or interfere with the function of hormones in the body. Endocrine disruptors may turn on, shut off, or modify signals that hormones carry,…. In 2000, an independent panel of experts convened by NIEHS and NTP (National Toxicology Program) found that there was credible evidence that some hormone-like chemicals can affect test animals’ bodily functions at very low levels — well below the “no effect” levels determined by traditional testing......People may be exposed to endocrine disruptors through …. the diet, air, skin, and water" (emphasis added) (5)
Continuing, "Research shows that endocrine disruptors may pose the greatest risk during prenatal and early postnatal development when organ and neural systems are developing. Endocrine disruptors can bind to a receptor within a cell and block the endogenous hormone from binding. The normal signal then fails to occur and the body fails to respond properly. Examples of chemicals that block or antagonize hormones are anti-estrogens and anti-androgens…. (They also can) interfere or block the way natural hormones or their receptors are made .....”
According to the Committee on Developmental Toxicology of the National Academy of Sciences, ”Agents that interact with one or more of these receptors and are known to produce abnormal development include ……dioxin (TCDD).<<checkothers>> The mechanism by which TCDD induces developmental toxicity has been studied extensively (for a review, see Wilson and Safe 1998) and is one of the best understood. It ….. alters the expression of several dozen genes, one or more of which might result in an adverse developmental outcome." (6) (emphasis added) Given that there are various different genes that guide the growth of different parts of the brain, exposure to a toxin that ”alters the expression of several dozen genes" can help explain why the autism spectrum disorders and other neurological damage can take many different forms.
From one of the EPA's documents on dioxins, (7) "Some of the effects of dioxin and related compounds such as …. changes in hormone levels and indicators of altered cellular function have been observed in laboratory animals and humans at body burdens comparable to exposures at or near levels to which segments of the general population are exposed." (emphasis added) It will be explained in the next section that any effect of changing hormone levels can be hazardous to development of the brain. Later in the same EPA document, it is spelled out that the adverse impacts that can occur as a result of relatively typical exposure to dioxins include impacts on "developmental and/or reproductive biology". The authoritative recognition that (probably harmful) effects of dioxins have been observed in humans at or near levels of substantial human exposure is of special significance in light of the following: A study in the Netherlands has found that breast-fed infants have a 50-fold higher daily dioxin intake than adults after adjusting for body weight. (d8, p. 7).
The U.S. Agency for Toxic Substances and Disease Registry says that dioxins are normally found in the environment in "… ash, soil, or any surface with a high organic content, such as plant leaves."(7b) The ATSDR and the EPA point out that dioxins are released by municipal solid waste and industrial incinerators, hospital waste incinerators, backyard burning, vehicle exhaust (mainly of diesel vehicles), emissions from oil- or coal-fired power plants, soil erosion and surface runoff. Note that most of the above sources are related to population density and human activity.
The EPA reports that major sources of dioxins in the environment have declined greatly in recent decades as a result of regulatory efforts, but some major sources have been increasing at the same time, especially diesel emissions and landfill emissions; and in any case dioxins are extremely persistent in the environment, especially in soil. Also, even the reduced levels of dioxins are still extremely high by historic standards: Estimates based on studies suggest that rates of dioxin deposition increased more than 10-fold from the 1930's to a peak in the late 1960's.(Regulatory Toxicology and Pharmacology, 37 (2003) 202 217 Dioxin risks in perspective: past, present, and future Hays and Aylward accessd at http://acdrupal.evergreen.edu/envirohealth/system/files/Dioxin+risks+in+perspective.pdf) Since formation of dioxins requires presence of chlorine during combustion, and since plastics are an extremely common source of chlorides in the waste stream that grew tremendously in the twentieth century, that is probably behind the huge increase in dioxin releases that took place during that period. Emissions from municipal waste combustion, medical waste incinerators, and secondary copper smelting have been leading sources of releases of dioxins to the U.S. environment, according to the EPA (EPA/600/P-03/002F November 2006 An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000) The 20th-Century explosion of plastics in our society made available ample chlorine to the municipal and medical incineration, and plastic insulation around copper that is being recycled has provided the chlorine that caused major dioxin releases from the secondary copper smelting. Regulatory efforts succeeded in reducing those sources of dioxins, but backyard burning (including its typical major component of plastics trash) is more difficult to control. So backyard burning has become the largest source of dioxin releases in the U.S. environment as of the latest EPA inventory (for year 2000)(above source, Table 1-4). The worst effects of the pollution generated would be on infants and child-bearing women living in the areas near where the burning is done, but the dioxins released would also enter the food chain of the general population (this burning is mostly done in rural areas). The emissions released would also be deposited on soil, water supplies, and in the form of dust, to which all infants downwind could be exposed.
In addition to possible or known endocrine-disruption properties, at least some PAHs are known to be potent mutagens (EPA/600/8-90/057F May 2002, Health Assessment Document for Diesel Engine Exhaust, Table 2-22. National Center for Environmental Assessment, Office of Research and Development, EPA). In addition, even after some PAHs degrade, many of their derivatives, also, "have been found to be highly mutagenic." (same EPA source, p. 2-90) Mutagens should be of special concern because they can affect the descendants of a person who outwardly appears to be unaffected. Later in this paper there will be various references to possible effects of environmental toxins on pregnant women and developing infants, and for brevity the possible effects on the genetic material in future parents of both genders will not be mentioned at the same time. But it should be kept in mind that mutagens could be affecting genes of both men and women now in ways that may not be apparent in them but which could be expressed in their future children.
Aside from the general knowledge about the presence of dioxins (and therefore endocrine disruptors) in many typical types of combustion emissions, research has specifically observed endocrine disruption resulting from exposure to diesel exhaust, which contains dioxins (see Section 1.4).
One specific means by which dioxins harm development of the brain is by their effect on thyroid hormones. "A number of studies indicate that dioxins and dioxin-like compounds decrease circulating thyroid hormone levels. A reduction of maternal serum thyroxin (T4) levels can impair the brain development of the offspring (Glorieux et al., 1988; Rovet et al., 1987; Haddow et al., 1999)." (Prioritization of Toxic Air Contaminants -- Children's Environmental Health Protection Act (State of California), October, 2001).
There will be reference later (Figure 13g in Section 4.2.c) to PCBs, some of which are "dioxin-like compounds" (closely-related chemicals that may sometimes be referred to simply as dioxins). Their importance lies in the fact that "one-third of general population TEQDFP (dioxin toxic equivalency) exposure is due to PCBs."* *(EPA/600/P-03/002F, November 2006: p. 11-28)
To summarize: Endocrine disruptors and mutagens can produce adverse neurological effects, especially during the period when the brain is developing. Some of these effects can take place at or near relatively frequently-occurring background levels. Infants are often likely to ingest or absorb toxins at far higher levels than adults, adjusted for body size.
1.2.b.1 The Special Significance of Testosterone/Androgens in Development of the Brain, and Window(s) of Sensitivity
It is important to look into the specific hormones that, when subject to the effects of endocrine disruptors, can fail to perform important functions in neurological development. According to one expert, "Sex steroid hormones (testosterone in males, estradiol and progesterone in females) play a role early in brain development in the "organization" of neural circuits… A wide variety of neural processes are influenced by sex steroid hormones, including neurogenesis, …growth of the neuronal cell body, dendritic growth, differentiation and synapse formation….and neuronal excitability. "(8) (italics added)
According to another specialist, B.S. McEwen, ”Gonadal, adrenal, and thyroid hormones affect the brain directly, and the sensitivity to hormones begins in embryonic life…. ….any agent that disrupts normal hormone secretion can upset normal brain development. Likewise, exogenous substances that mimic the actions of natural hormones can also play havoc with CNS (central nervous system) development and differentiation." (9) It may be noteworthy that gonadal hormones are the first of the various types mentioned by the author regarding their importance to the developing brain.
Other authors (S.B. Klein and B.M. Thorne) (10) point specifically to testosterone for the way it "clearly affects brain development." They refer to the "critical period for the testosterone organizational effect" which apparently can take place only within a limited window of time while the brain is developing. They cite observations of male rats that are castrated after birth to remove their normal principal source of testosterone, followed by injections of testosterone at various later times. Injections of testosterone during the first two days after birth were effective in leading to some specifically male rat behavior when adulthood was reached. But the effectiveness of the replacement hormones in promoting normal male brain development rapidly declined to "little effect" when not administered until 13-14 days after birth. Other researchers have said that "Androgens are thought to organize the male brain"(11b) (testosterone is one of the androgens).
McEwen points out that testosterone has a developmental influence on the cortex (the part of the brain that plays a key role in memory, attention, perceptual awareness, thought, language, and consciousness).(9) Klein and Thorne also cite observations by Rhees and colleagues (1990) and Davis and colleagues (1995) of structural differences in adult rats' brains depending on presence or absence of testosterone at specific stages of early infancy.
It should be pointed out here that, although testosterone is a predominantly male hormone, females also have testosterone in their bodies, just much less of it than males (about one tenth as much in infancy). It is important to providing mental as well as physical energy and to development of the female brain also. (Notice that the quotes about testosterone's influence in brain development, above, don't specify just the male brain).
The validity of the concept of "critical windows of sensitivity" during neurological development is also accepted by the National Research Council of the National Academy of Sciences (14), and by authors writing for the EPA(15). Wigle et al. refer to biomolecular research showing the dependence of fetal and child development on a complex orchestration of genes in specific cell types at different times.(16)
The importance of testosterone in infant brain development may help explain why far more boys than girls become mentally disabled, since testosterone's production is extremely vulnerable to disruption in male infants. It is produced in endocrine glands (testicles) that are uniquely exposed to effects of toxins in air, water, and diapers, often shielded on almost all sides by nothing more than a thin, permeable enclosure which provides only minimal protection from microscopic substances in the surrounding area. All of the other endocrine glands have far greater shielding from environmental toxins. Exposure of the testicles to toxins from the environment is greatly amplified during the critical brain development period by the fact that infants are normally bathed in tubs, promoting soaking into the scrotum of substances that may have been (a) deposited into the tub from the air, cleaning agents, or runoff from shower curtains, (b) gathered onto the infant's body from the air, dioxin-containing diapers or soil, and/or (c) brought in via the water supply. The same exposure of the testicles to dioxins (and other toxins) could take place when a boy spends time in a swimming pool or pond into which the toxins have settled out of the atmosphere.
When considering the last sentences above, it is worth remembering from the preceding text the following:
(a) dioxins and at least one PAH are endocrine disruptors, which are known to (among other things) interfere with secretion of hormones;
(b) endocrine disruptors can be absorbed from the environment through the skin, and
(c) ”…any agent that disrupts normal hormone secretion can upset normal brain development."
Winter and colleagues plotted hormone levels in boys during
normal postnatal development, showing relatively high levels of male
hormones during part of infancy, before the hormones decline to the
prepubertal range.(17) This should receive very special attention, since
those high levels at this stage are apparently not for purposes of
stimulating reproductive development. But as explained earlier in this
section, male hormones do promote proper development of the male
brain during infancy. And that crucial activity (binding to receptors in
the brain to cause proper neurological development) is extremely vulnerable
to interference by environmental toxins. The above researchers refer to a four-month post-natal period
after which the male hormones decline to the pre-pubertal level. The
timing as shown here could help determine when the "critical
window(s)" occur, during which neurological development could be
obstructed by interference with creation of male hormones or by
interference with connections of hormones to receptors in the brain.
Fig.
1.2

Should it be surprising that four to five times as many boys as girls are diagnosed with autism (18), considering that
a) development of the brain depends on the undisrupted effects of certain hormones (see early paragraphs of this section), and
b) those specific, crucial hormones are produced in boys in a location that is uniquely and extremely vulnerable to harm by external toxins?
In an article authored by a PhD at the CDC, it was pointed out that some recent studies have identified male-to-female ratios of autism as being double the four-to-one ratio often indicated in older studies.(17b). That provides reason for added focus on toxins that specifically affect male infants more than females.
Although the above discussion focuses mainly on the very early life of a child (since that is the period of greatest neurological development), it should be pointed out that development of the brain continues into early adulthood <<ref>>, which means that serious attention should also be paid to minimizing time during which the scrotum of a developing boy soaks in water that could contain dioxins, which is to say most outdoor pools and lakes. The same applies to bromine, which is a known neurological toxin (http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1246260027938 (HPA is Health Protection Agency of the UK) Bromine Toxicological Overview) that has been coming into wider use as a substitute for chlorine in swimming pools and spas. Like dioxins, bromine can be absorbed through the skin. (www.newsmaxhealth.com, Dr. Brownstein)
Aside from their role as endocrine disruptors in general, dioxins are known to affect male endocrine glands specifically, that is to say affecting the source of the testosterone that is essential to normal infant male brain development. According to another CDC report, dioxins have been demonstrated in animal studies to have effects including neurotoxicity, teratogenicity (causing birth defects), altered transcription of genes, altered thyroid function, and testicular atrophy. (National Report on Human Exposure to Environmental Chemicals Dioxin-Like Chemicals: Polychlorinated Dibenzo-p-dioxins, Polychlorinated Dibenzofurans, and Coplanar and Mono-ortho-substituted Polychlorinated Biphenyls Centers for Disease Control and Prevention Atlanta, GA Accessed at http://www.cdc.gov/exposurereport/data_tables/DioxinLikeChemicals_ChemicalInformation.html Page updated April 2010) According to researchers for the EPA, "In tests by at least two different research teams, dioxins were found to have effects on the male reproductive systems in rats tested, as follows: impaired testosterone synthesis, and possibly central nervous system sexual differentiation, feminization of male sexual behavior." (Environmental Endocrine Disruption: An Effects Assessment and Analysis, by Thomas Crisp et al, EPA, in Environmental Health Perspectives, Vol. 106, Feb. 1998, Supplement. P.27) " Scientists at the University of Wisconsin, on the basis of testing of rats, found that "if TCDD (dioxin) interferes with any of (various) processes during late gestation and/or early neonatal life, it could irreversibly demasculinize and feminize sexual behavior…in male rats in adulthood.(Developmental and Reproductive Toxicity of Dioxins and Related Compounds: Cross-Species Comparisons" Richard E. Peterson et al, School of Pharmacy and Environmnental Toxicology Center, Univ. of Wisconsin EPA/600/J-93/470 Critical Reviews in Toxicology, 1993) "In mammals, postnatal functional alterations involving learning behavior and the developing male reproductive system appear to be the developmental events most sensitive to perinatal dioxin exposure."(Crisp et al., p. 324) The specific mechanism by which dioxins cause neurological harm to infants is by changing thyroid levels: "Even low levels of dioxin or PCB exposure during the perinatal period can greatly influence neurological development by the effects of these chemicals on thyroid levels in the developing brain." During the development of the brain, "a lack or excess of thyroid hormone arising at specific stages can cause irreversible neurological damage." (Industrial Health 2000, 38, 259–268 Review Article The Effects of Dioxin on Reproduction and Development Junzo YONEMOTO National Institute for Environmental Studies, 16–2, Onogawa, Tsukuba, Ibaraki 305-0053, Japan p. 262)
Dioxins have been found in bleached paper products, which include disposable diapers, usage of which has been becoming far more widespread during the same recent decades during which autism has also been increasing rapidly. In that regard, keep in mind again that
a) dioxins and some other endocrine disruptors can be absorbed through the skin, and
b) glands that produce hormones which are important to male brain development are uniquely exposed to toxins that can be absorbed through skin.
1.2.b.2 Major types of PCBs, as mentioned, are considered to be "dioxin-like" and are often referred to simply as dioxins. There is clear evidence from research involving humans (to follow) that moderate, background-type exposure of infants to PCBs harms mental development. The following is taken from a State of California website. ("Prioritization of Toxic Air Contaminants: Dioxins" - Children’s Environmental Health Protection Act October, 2001 (State of California) At http://oehha.ca.gov/air/toxic_contaminants/pdf_zip/dioxin_Final.pdf, p. 17 ff). Various researchers "have reported persistent neurological effects" of PCB exposures. Another study, with 395 children, "reported that exposure in utero to 'background' PCB concentrations is associated with poorer cognitive functioning (cognitive abilities and verbal comprehension) in preschool 42-month-old children." Another study, of 212 eleven-year-olds, involved children born to mothers who were known to have consumed Lake Michigan fish contaminated with PCBs, comparing them with a control group without such exposure. The study found that the most highly-exposed children were "three times as likely to have low average IQ scores and twice as likely to be at least two years behind in reading comprehension." (emphasis added) Other strong effects were related to memory and attention.
Many major sources of releases of PCBs to the environment have been discontinued, which helps explain the major decline in mental impairment among girls born in recent decades. But some sources remain, and in any case they are extremely persistent in the environment. And since PCBs, specifically, have been found to harm neurological development, that lends additional weight to the evidence that the other dioxins (or "dioxin-like" chemicals) still in widespread emissions would have similar effects.
1.2.c Even Low Exposure to Dioxins can Cause Developmental Harm: Media attention regarding dioxins normally centers on their cancer-causing effects (which are either "known" or "probable" depending on which particular governmental body is speaking). But close reading of the CDC's web pages on dioxins will reveal statements indicating that dioxins are also closely connected with developmental harm, even at low doses. "The results of the oral animal studies suggest that the most sensitive effects (effects that will occur at the lowest doses) are immune, endocrine, and developmental effects." (found at http://www.atsdr.cdc.gov/phs/phs.asp?id=361&tid=63 , Section 1.5) The CDC web page continues: "It is reasonable to assume that these (effects of low dioxin doses on development, as observed in animals) will also be the most sensitive effects in humans."
1.2.d Human Breast Milk as Sources of Toxins to Infants: <<coordinate w/ Sec. 1.9.11, 1.9.9?>> According to the National Academy of Sciences, a leading U.S. government regulatory agency points out regarding dioxin exposure from breastfeeding that " the average daily intake by the infant over the first year of suckling would be 87 times the adult daily intake." The NAS apparently saw no reason to disagree with that estimate. (National Academies Press: Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment (2006), Board on Environmental Studies and Toxicology, National Academy of Sciences; the original source is not quoted directly because it is part of a draft, not for quoting) Many studies have found health benefits in breastfeeding, so the best course would probably be for the mother to start years before birth to minimize her consumption of mercury and dioxins (which are especially high in meat, animal fats and many types of seafood), so as to minimize the toxins in her milk.
But, if a mother has been consuming a fairly typical American diet, she should carefully consider the risks of the toxins that are within her milk, and think about alternatives to breast feeding. "Breast-feeding for 6 months or more is predicted to result in an accumulated (dioxin) exposure 6 times higher than a formula-fed infant during the infant's first year of life.." (EPA Home/Research/Environmental Assessment: An Evaluation of Infant Exposure to Dioxin-Like Compounds in Breast Milk) Also note the following quote from a web page of the State of California OEHHA: "Current background levels of human exposure to dioxins in particular are within the range at which various toxic responses have been observed in animals." (in Prioritization of Toxic Air Contaminants - Children’s Environmental Health Protection Act, October, 2001: Dioxins ) Current background levels of dioxins therefore are such that toxic effects can be expected in humans, based on studies with animals. And breastfeeding infants, with their special vulnerability as their brains are developing, and with their incomplete defense mechanisms, are receiving exposure that vastly exceeds that of the average adult. Not to mention the fact that some humans are far more sensitive to toxins than others.
In order to appreciate the fact that typical breast milk in nursing mothers these days is very different from that in earlier times, one should be aware of the following:
1) Estimates from various studies suggest that rates of dioxin deposition in the environment (mostly from the air) increased more than 10-fold between1930s and the late 1960s. (Regulatory Toxicology and Pharmacology, 37 (2003) 202 217 Dioxin risks in perspective: past, present, and future Hays and Aylward at http://acdrupal.evergreen.edu/envirohealth/system/files/Dioxin+risks+in+perspective.pdf ) Mercury deposition has also increased substantially, and continues to rise.
2) The American Toxic Substance and Disease Registry says that "eating food, primarily meat, dairy products, and fish, makes up more than 90% of the intake of CDDs for the general population." (http://www.atsdr.cdc.gov/toxfaqs/tf.asp?id=363&tid=63) Farm animals and fish ingest and build up dioxins in their tissues largely as a result of what they eat, meaning vegetation and sediment onto which the greatly-increased levels of dioxins and mercury from the environment have been deposited; in addition there is "biomagnification" (via animal products included in the feed of farm animals, and also via smaller fish being eaten by larger fish).
3) "Meat consumption has more than doubled in the United States in the last 50 years." ( "Paying a Price for Loving Red Meat" in Personal Health, by Jane E Brody, New York Times: April 27, 2009)
4) Regarding dairy products as sources of dioxins, it should be emphasized that fat is the component of animal matter to which dioxins especially gravitate. Therefore butter, eggs, most cheeses, and whole milk, as well as lard (commonly found in bakery products) are very much on the list of significant sources of dioxins in a typical diet. Although most dairy foods may not have been increasing substantially in quantity in the average diet, their average dioxin content per ounce is much higher than in earlier times, following the increases of the toxins in the environment. That is especially important for people whose typical meals are high in dairy fat content, such as is apparently the case in Scandinavian diets.
In addition to the previously-mentioned special vulnerabilities of infants to toxins, their brains are particularly subject to damage by dioxins, for the following reason: Dioxins are "lipophilic" (attracted to fat, which is the major content of nerve tissue, including the brain). "Lipophilic xenobiotics (chemical compounds foreign to the organism) may more readily penetrate the central nervous system in infants and young children until the blood-brain barrier reaches maturity in the third year of life." (The symptoms of autism are typically observable before age 3, so the brain may well have already been permanently damaged by incoming toxins before the blood-brain barrier has matured.) Also, "...infants may have decreased excretion and clearance of xenobiotics, prolonging half-life and potentially increasing toxicity." (parenthetical expressions added) (Protecting Children from Harmful Chemical Exposures Chemical Safety and Children’s Health Prepared by: IFCS FSC Working Group Chaired by Hungary Chemical Safety in a Vulnerable World IFCS/FORUM-IV/11 INF 7 October 2003 FORUM IV Fourth Session of the Intergovernmental Forum on Chemical Safety Bangkok, Thailand, p. 9 accessed at http://www.who.int/ifcs/documents/forums/forum4/en/11inf_en.pdf) Some agencies downplay the significance of the extraordinarily high dosage of dioxins received by infants in breast milk, pointing out that, if one looks at that dosage spread out over a typical 70-year lifespan, it becomes a relatively minor addition to the typical total lifetime exposure to dioxins. The problem with that viewpoint is that permanent, life-impairing damage can often occur during infancy while exposure levels are many times higher than the later lifetime average, early levels that are especially high in relation to the infant's immature defense mechanisms.
Dioxins are far from the only neurological toxin of concern contained within breast milk. Quoting from page 12 of the above IFCS FSC Working Group paper, "Heavy metals such as methylmercury and lead are also secreted in breast milk." Other chemicals that have been rapidly increasing in the environment just in recent decades and which are also of special concern are PBDEs.(Polychlorinated Biphenyls (PCBs) and polybrominated diphenhyl ethers (PBDEs) in milk from Italian women living in Rome and Venice", Ingelido et al., Chemosphere, Vo. 67, issue 9, April 2007, obtained from Air Force Institute of Technology, ILL. "Several toxic effects on the thyroid system or on neurodevelopment have been reported in experimental animals exposed to PBDEs. It is likely that human exposure is predominantly through the ingestion of contaminated food and/or mother's milk." ((Shokuhin Eiseigaku Zasshi. 2004 Aug;45(4):175-83. PubMed – NCBI Polybrominated diphenyl ether flame retardants in foodstuffs and human milk. Akutsu K, Hori S. Osaka Prefectural Institute of Public Health: 1-3-69, Nakamichi,Osaka 537-0025, Japan) Remember from Section 1.2.b.1 that increases or decreases in thyroid levels have been reported to "cause irreversible neurological damage" during development of the brain. Also note, as will be mentioned in Section 1.7.1, that samples of breast milk in the U.S. were found to have levels of PBDEs 10 to 100 times as high as those found in humans in Europe. Bromine is another neurological toxin excreted in breast milk (CAS No: 7726-95-6) Health-based Reassessment of Administrative Occupational Exposure Limits, Committee on Updating of Occupational Exposure Limits, a committee of the Health Council of the Netherlands); bear in mind that a mother could absorb bromine through her skin while in a pool or spa treated with bromine as a disinfectant.
Pesticides also, including some that are used residentially, have been widely found in breast milk. (http://ehpnet1.niehs.nih.gov/docs/2001/109p75-88lakind/abstract.html Environmental Health Perspectives, Vol. 109, No.1, Jan. 2001). Section 1.6.1 will provide details about connections between various pesticides to which fetuses and infants are exposed and (a) autism, (b) other changes in social behavior and brain development, (c) attention deficit disorders and hyperactivity disorders, (d) feminization of males and (e) masculinization of females.
1.2.e Connections between Varying Rates of Breast Feeding, Various Social Characteristics, and Autism Prevalence
Among families with certain social characteristics, there are both far higher rates of breastfeeding and substantially higher rates of autism. Those characteristics are (1) high levels of education, (2) white as opposed to black ethnicity, and (3) (probably) white as opposed to Hispanic ethnicity. Education: The CDC shows an 87% higher rate of breastfeeding among college graduates as opposed to high school graduates at 6 months after birth, and 100% higher at 12 months.(http://www.cdc.gov/breastfeeding/data/NIS_data/2000/socio-demographic.htm ) An in-depth study of autism in California "…showed autism clusters to be highly associated with the education of the parent population" (meaning higher autism in areas with higher educational levels). The research team looked at many other environmental factors that could have been associated with formation of the clusters, but "…none of the effects approach the magnitude of parental education." The authors pointed out that services for the autistic were available regardless of income, so ability to pay was not seen as something to reduce use of autism-treatment services by less-educated families. To summarize the above: 87%-to-100%-higher rates of breastfeeding among college graduates vs high school graduates, and prevalence of autism strongly associated with parental education levels, with the two associated in a magnitude that no other environmental factors could approach.
Low income levels, closely associated with low educational levels, also go along with low rates of breastfeeding. (Couples' Immigration Status and Ethnicity as Determinants of Breastfeeding Christina M. Gibson-Davis, PhD; Jeanne Brooks-Gunn, PhD American Journal of Public Health. 2006;96(4):641-646).
Fig. 1.3
Ethnic differences: The
CDC shows rates of breastfeeding among blacks or
African Americans at 6 and 12 months after birth as being about half as high as
among whites (http://www.cdc.gov/breastfeeding/data/NIS_data/2000/socio-demographic.htm
).
And autism rates among blacks are also about half as high as among whites, as
reported by many sources.
Hispanics: U.S. Hispanic rates of breastfeeding, overall, are reported by a telephone survey to be very similar to those of whites. But since the survey was conducted by calling only families with landline telephones (Racial and Ethnic Differences in Breastfeeding Initiation and Duration, by State --- National Immunization Survey, United States, 2004—2008 CDC Weekly March 26, 2010 / 59(11);327-334), the results almost certainly under-reported practices of families with low incomes, therefore disproportionately under-reporting Hispanic families with low rates of breastfeeding. (Remember from above that low-income families are likely to have lower rates of breastfeeding.) Also, since the legal residency in the U.S. of many Hispanics is not established, there was probably a tendency for such respondents to provide answers that indicate compliance with practices that are apparently favored by the government. Therefore the reported similarity of breastfeeding rates of Hispanics and whites is at minimum subject to serious question. And, given the above questions along with the well-established association of lower breastfeeding rates with lower educational levels, it is very likely that actual breastfeeding rates of U.S. Hispanics are lower than those of whites. In that regard, note in Figure 1.3 that ASD rates among U.S. Hispanics are also lower than those of whites.
The above-mentioned survey by the CDC reported breastfeeding rates in California, specifically, to be about 18% lower among Hispanics than among whites. (http://www.dds.ca.gov/Autism/docs/AutismReport_2007.pdf) In line with that, the state of California reports that 36% of Californians are Hispanic, but only 28% of those with diagnoses of autism are Hispanic. (That is the only individual-state breakdown of Hispanic vs. white rates of breastfeeding that this author has found so far.)
Irish breast-feeding rates are by far the lowest of any major people in Western Europe or North America. (Data provided by LaLeche League for Northern Ireland, accessed at http://www.lalecheleague.org/cbi/bfstats03.html, in line with data for Dublin area from Public health nutrition. Breast-feeding practices in Ireland, Tarrant RC, Kearney JM., School of Biological Sciences, Dublin Institute of Technology, Republic of Ireland, accessed at Proc Nutr Soc. 2008 Nov;67(4):371-80. Epub 2008 Aug 20.) And Irish rates of autism also appear to be well below average. Irishhealth.com reports autism prevalence in Ireland to be one out of 166 (Research to determine autism incidence [Posted: Fri 03/04/2009 by Deborah Condon www.irishhealth.com]), compared with a rate of about one out of 110 in the U.S.
The low rate of autism among the Irish probably has nothing to do with any ethnic advantage (see the high "White, Non-Hispanic" rate of autism in Figure 1.3). The above may help explain why certain U.S. areas that have high Irish ancestry and high minority populations (like the New York City area) have relatively moderate levels of autism, despite relatively high risk for neurological impairment on the basis of atmospheric pollution.
Fig.
1. 4
Scandinavians: Autism symptoms were identified in an exceptionally high 2.7% of children in Norway in one study, as indicated in an article by a researcher with the CDC. (http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5810a1.htm ) In that regard, note the straight line at the top of this chart, which is the breastfeeding rate for Norway exceeding the highest level on the chart, but represented only by that maximum line as shown. Sweden was another country indicated by the above-cited author as having an unusually high rate of autism, and Sweden's rate of breastfeeding can be clearly seen in the second-from-highest line on this chart.
There is good reason why organizations that promote breastfeeding present Norway as the international example to follow. But such organizations may not know that Norway also stands out with what may be the highest rate of autism in the entire world; or they probably aren't aware of the good scientific reasons implicating high levels of breastfeeding in modern industrialized countries with neurological impairment.
Fig. 1.4a

The maps shown here (files from the Wikimedia Commons, apparently drawing on U.S. Census 2000 data. Found in Wikipedia under "Maps of American Ancestries"), indicating concentrations in Minnesota of descendants of Norwegian and Swedish immigrants, help illustrate apparent effects of different levels of breastfeeding by mothers with alternative dietary habits. As could have reasonably been predicted from the fact that breastfeeding rates are very unusually high in Norway and Sweden, the highest American levels of breastfeeding (being culturally-influenced) are found in Minnesota and very few other states.(CDC data found at http://www.cdc.gov/breastfeeding/data/NIS_data/) Knowing the developmental toxins concentrated in the breast milk of the typical U.S. mother (see Section 1.2.d), it should not be surprising that prevalence of autism in Minnesota is the highest in the U.S. (IDEA data, averaging years 2005-2008 -<<show more detail>>) . And not just moderately higher than the average: More than twice as high as the median for the U.S. states.
When observing the above, remember also that the mother countries, Norway and Sweden, both with unusually high rates of breast feeding, were found to be either extremely high in autism level (Norway) or unusually high (Sweden).
With a breastfeeding rate even higher than that of Minnesota, the state with the very highest rate of breastfeeding in the U.S. is Oregon, which also has the second-highest rate of autism in the U.S., at almost exactly twice the national median.
Section 1.2.f Dietary and Other Factors that Tie in with Breastfeeding, affecting Toxin Levels in the Milk
As has been noted, diet (mostly animal-based fats) is considered by the EPA and ATSDR to be the source of about 90% of the average body burden of dioxins. Typical Scandinavian cuisine would normally only add to the levels of dioxins in breast milk consumed by infants in Minnesota. Recipes for favorite traditional Norwegian dishes (easily found with a web search) show very high animal-fat content, especially butter. Swedish cuisine is very similar to that of Norway (http://recipes.wikia.com/wiki/Swedish_Cuisine). An article in The Canadian Physician (VOL 39: January 1993)refers to ”the very high level of cholesterol and fat in the normal Scandinavian diet," The only comment found on the subject of intergenerational transmission of culinary traditions includes the following: "WHEN I WAS OLD ENOUGH MY GREAT GRANDMOTHER STARTED TO TEACH ME THE OLD WAYS OF COOKING IN SWEDEN ….TODAY AT 59 YEARS OLD I STILL MAKE THOSE DISHES THAT MY GREATGRAND MOTHER TAUGHT ME AS A YOUNG CHILD."(same source as above) That sort of maintenance of cultural traditions would be especially likely to hold sway in communities where there are concentrations of people with common ancestry (as shown in the above maps), along with Lutheran church festivities and other vehicles that promote continuation of an ethnic heritage. It also makes sense that a diet high in fat -- an excellent source of energy for keeping warm, which promotes comfort during long, cold winters in the (very northern) old country -- would be continued in a new cold domicile in the U.S.; Minnesota has 17 of the nation's coldest 21 cities with populations over 50,000 (City-Data.com) Supply of dairy products in Minnesota is also very ample, keeping prices down and encouraging consumption: The region consisting just of Minnesota and its neighbor Wisconsin produces more milk than any of the other three USDA regional groupings of major dairy states in the eastern and southern two-thirds of the U.S. (USDA data found at http://www.ers.usda.gov/publications/err47/err47b.pdf)
So it is probably safe to assume that consumption of dairy products and fat is unusually high in Minnesota. And knowing what was stated earlier about dairy products and animal-based fats as sources of dioxins in humans, it is very likely that dioxin content in typical breast milk in Minnesota is unusually high. That could only contribute to the likelihood that the high level of breastfeeding in Minnesota is causally connected with that state's place at the very top of U.S. states in prevalence of autism.
As pointed out earlier (Figure 1.3 and accompanying text), rates of autism among Hispanics are significantly lower than among whites. That is partly associated with what is probably a lower rate of breastfeeding among Hispanics, and partly connected with the way the Hispanic diet differs from the typical American diet, which in turn affects the levels of toxins in the typical Hispanic breast milk. Compared with whites, Hispanics are reported to purchase less dairy products and snack foods, such as potato chips, candy, and cakes. (At http://www.faqs.org/nutrition/Pre-Sma/Regional-Diet-American.html) Remember from above the importance of dairy products and fats (such as are at high levels in most snack foods) as sources of dioxins in the diet.
Section 1.2.g The Case of Washington State: Back to the subject of regional variations in diet and the effect of those variations on toxins in breast milk: Prevalence of breastfeeding in Washington state is very high; but reported autism rates in this case are much lower than those reported for Minnesota and Oregon, departing from the (simplified) pattern that has been discussed so far. There are good reasons for this deviation, as follows:
1) Noticing the far lower levels of Norwegian and Swedish ancestries in Washington than in Minnesota, it is reasonable to expect dioxin ingestion from dairy fat consumption to be much lower in that state;
2) Regarding the other largest sources of dioxin and mercury body burdens (meat and fish), it is significant that there are over 2 ½ times as many vegetarian restaurants per million population in Washington as in Minnesota (www.happycow.com and U.S. Census Bureau data);
3) Regarding the general environmental pollution that underlies toxin levels in much of Washington's food supply, and regarding the pollution levels that affect what mothers and infants in that state breathe, absorb and ingest directly, note the following:
The State of Washington is very unusually strong in preventing pollution:
-- Bearing in mind that residential wood burning is a known substantial source of emissions of dioxins, particulate matter and lead, note that Washington prohibits outdoor wood boilers and has very strict regulations about other residential wood burning; there are residential "burn bans" if pollution exceeds a certain level.(d83c). A search for regulations on websites of other state governments' environmental agencies (especially including the high-autism states) yields nothing of similar forcefulness. Three of Washington's publications regarding wood smoke pollution are of such recognized quality that they are recommended reading even on a state environmental website from distant Minnesota.(d69b)
-- A detailed 2010 study of pollution levels in Washington's Puget Sound found that most contaminants were at far lower levels than had been projected, some by as much as 99%; and the study's lead researcher concluded that "Regulations and increased public focus on pollution prevention appear to be paying off."(d69c)
-- The above are merely examples, which are no doubt representative of many other aggressive actions taken by the Washington Department of Ecology that promote low levels of toxins in the environment. And it is unlikely that a state's environmental department would be so unusually active and effective unless many of the state's citizens were supportive of efforts to reduce pollution.
There should be little doubt that such unusual legal requirements (and probable public involvement) have substantially reduced emissions of developmental toxins in Washington. And those actions appear to stand out in comparison with the lack of such measures on the parts of the states that, in contrast with Washington, have the very highest rates of autism.
So therefore the association of autism with high levels of breastfeeding obviously needs to be refined. High levels of autism appear to be associated with high levels of breastfeeding in an area if there are reasons to expect women's body burdens of dioxins and mercury to be typical or high in that specific area.
Section 1.2.h Possible Sexual-Orientation Effects of Dioxins in Breast Milk
In 1981, Norway became the first country in the world to enact anti-discrimination laws protecting gay men and lesbians under both civil and criminal legislation.(http://www.glbtq.com/social-sciences/norway.html ) This "first" was not for lack of a Christian influence in that country; the Church of Norway claims about 86% of the population as baptized members.(http://www.kirken.no/english/engelsk.cfm?artid=5730). It is very possible that it was merely a bow to political reality in a democratic country with a large gay population. Probably many voters have gay fellow workers, relatives and/or friends, and the resulting familiarity caused most people to realize that gay people are good citizens and worthy human beings, not deserving of being discriminated against. It is also likely that a large gay population is associated with Norway's unusually high rate of breastfeeding, given the high levels of certain ingredients typically present in breast milk in modern industrialized countries, including ones found to cause feminization in sexual behavior of male laboratory animals (see Section 1.2.b.1).
Sweden "is one of the most gay friendly nations on earth" with considerable legislation protecting gay and lesbian rights; "businesses face up to one year’s imprisonment if they fail to provide their normal level of service to someone because of his/her homosexuality."(http://www.gaytimes.co.uk/Hotspots/GayGuide-action-Country-countryid-912.html ) Again, unusually forceful national action favoring gays is probably related to an unusually large gay population within that nation. And again, it is a country with a high rate of breastfeeding that probably has the unusually large gay population.
Minneapolis, the capital of what is the most heavily Swedish/Norwegian U.S.state, with its confirmed very high rate of breastfeeding, was named Number 1 on the list of "Gayest Cities in America" by a gay-oriented publication. (http://www.advocate.com/Print_Issue/Travel/Gayest_Cities_in_America_February_2011/). In the absence of a census of the homosexual population, this publication did a study that was actually rather thorough when coming up with their list of the top 15 gay cities. They counted personal profiles placed on Gay.com for each city, numbers of elected openly-gay officials, performances by gay-oriented entertainers in the city during the previous five years, numbers of gay and gay-friendly religious congregations, lists of officiants for gay weddings, and other indicators of homosexual population size for each city, and then adjusted for the cities' population sizes. This is probably not only the best available index of the gay percentages of different cities' populations, it's probably also a reasonably accurate one. And Minneapolis, the capital of the state with by far the greatest concentration of the ethnicities that stand out with high rates of breastfeeding, is at the top of the list. But keep in mind that the probable effects of breastfeeding in Minnesota have to do not only with its prevalence but also with the likely contents of the breast milk; the high-fat Scandinavian diet increases the intake into women's bodies of the dioxins that have been found to feminize male laboratory animals (see Section 1.2.b.1) and possibly also toxins of the kind that masculinize female animals (see Section 1.6.1).
Washington state, one of very few states joining Minnesota on the list of states with the highest rates of breastfeeding, has two cities on the above-mentioned 15-city list of "Gayest Cities." That standing comes despite not having a large general population or a climate that is nearly as inviting as either of the other two other states (Florida and California) that each have two Gayest Cities.
Note that possible neurological effects of breastfeeding, seen to be possibly strong in Washington in this case, aren't in conflict with the previous finding that, in another area, the effects of breastfeeding were relatively weak. There are many different variations of dioxins (so-called "congeners") in the environment, with varying effects on neurological development; some of them are successfully minimized by Washington's anti-pollution efforts, and some of them are probably not so minimized, before they enter and accumulate in the bodies of mothers-to-be.
On the OECD chart farther down, only three of the many countries shown have higher rates than Norway and Sweden for breastfeeding four months after birth: Hungary, Slovak Republic, and Denmark. Denmark was the first country in the world to recognize marriage between two persons of the same sex, and Copenhagen (Denmark's capital) was named among the world's top 7 most gay-friendly destinations by "Hotel & Resort Insider". (http://www.visitdenmark.com/usa/en-us/menu/turist/inspiration/offersanddeals/gaytraveloffers/gay-travel-copenhagen.htm)
Seeing all these cases of specific geographic entities with unusually high rates of breastfeeding which are also exceptionally gay-friendly, one might reasonably consider the possibility that these coincidences are more than coincidental. Bear in mind what was pointed out earlier about findings in research with laboratory animals that showed exposure to dioxins (which are known to be highly concentrated in breast milk) contributing to de-masculinization or feminization of male animals.
(Note to readers: Please excuse the above digression from this paper's central topic of mental impairment. The above was included to help people realize that there is probably a connection between what is ingested by infants, including in breast milk, and the mental developments of the infants being fed. Referring to feminization of male sexual behavior as indicated by various scientific studies, and to gay friendliness in certain places, is not intended to imply that these characteristics should be looked on negatively; but most parents would want to know that there are good scientific reasons to suspect that a non-traditional sexual preference might be more likely to result from exposing their infant boys to chemicals that are known to be concentrated in typical current U.S. breast milk.)
Section 1.2.i PCBs, a "Dioxin-like" Toxin:
Fig. 1.5

The EPA does not provide data about total dioxin levels broken down by state, but it does provide a map showing levels of PCBs, many variations of which are "dioxin-like" and are therefore often referred to simply as dioxins. As noted earlier (Sections 1.2.b.1-2), PCB exposure (like that of dioxins in general) even at low levels during the perinatal periods is reported to be able to influence development in a way that can "cause irreversible neurological damage."
Oregon, as mentioned, has an
autism rate twice as high as the national median, and nothing stands out on
this map of PCB concentrations like the highly-populated part of Oregon. That specific
dark area is also the section of Oregon with the
highest levels of autism, within a high-autism state.<insert ref or
map>>There are also many paper and pulp mills in that same area, and such
mills are known sources of dioxins and other neurological toxins. So the
environment in which the average nursing mother in Oregon has been eating and
breathing seems to be unusual, and not in a good
way.
In this side-by-side map of Oregon, notice how similar the area with the most paper and pulp mills is to the area (in black) with higher-than-median levels of autism.
Maine is the state with the third-highest level of autism, and it is also another one of the states with very high levels of breastfeeding. The state also has unusually large numbers of paper and pulp mills (19, most of which include the more-polluting pulp operation)(http://www.cpbis.gatech.edu/data/mills-online?state=Maine).
One has to look closely in Figure 1.5 to see the small state of Vermont, which is essentially the un-colored section directly below the "a" in "Concentrations" in the map's heading. The lack of color in that thinly-populated, very non-industrial state's location on the map says something about the kind of environment in which Vermont's mothers live, and about the probably-low average levels of toxins in their breast milk. There is apparently only one company in Vermont with a paper and pulp mill (www.cpbis.com for Vermont). The above helps explain why Vermont can be among the states with the highest levels of breastfeeding while at the same time having a low level of autism.
Section 1.2.j Effects of Coastal Location: But there are, as usual, other factors that help explain the differences observed. According to a study of mercury levels in U.S. women by a researcher with the EPA and others, "Women living near the coastal areas had approximately three to four times greater risk of exceeding acceptable levels of Hg exposure than did noncoastal-dwelling women."(Adult Women's Blood Concentrations Levels Vary Regionally in the U.S., by Kathryn R. Mahaffey,1et al (1Office of Science Coordination and Policy, EPA) found at http://www.medscape.com/viewarticle/587407_4). That probably helps explain why the states with the second and third highest rates of autism in the U.S. (and very high rates of breast feeding) are states with the bulk of their populations near an ocean, while a landlocked state with high breastfeeding rates has relatively low autism. An earlier statement is worth repeating: High levels of autism appear to be associated with high levels of breastfeeding if there are reasons to expect women's body burdens of dioxins and mercury to be typical or high in that area. But it should be kept in mind that reasons for expecting high body burdens of toxins can be only partly shown by a map such as this one, or by considering distance from the coast. It is apparently, more than anything, a matter of individual long-term dietary habits
Section 1.2.k Other Sources of Pollutants: On the subject of low pollution and consequently low toxins in breast milk: The reader may have noticed in Figure 1.4 that the area with relatively high percentages of Norwegian and Swedish ancestry extends west from Minnesota into the Dakotas, especially to North Dakota. And rates of breastfeeding are also high in those states (although not as high as Minnesota's). But rates of autism in those two states are substantially below average. So it is worth looking at levels of pollution in those states, which are likely to end up in breast milk. Figure 1.5 shows almost total absence of PCBs where those two states are located. The American Lung Association in its 2009 "State of the Air" report ranked Fargo (the largest city in North Dakota) as the cleanest city in the United States, and gave the rest of the state 11 "A" ratings on air quality.(Wikipedia). Less than 2% of North Dakota's land area is forest land, meaning that firewood for residential burning would be especially expensive, reducing that potential source of particulate matter, dioxins and lead in the air to an extremely low level.
Fig. 1.6
In areas with substantial forest land such as Minnesota, Maine,
and the Pacific Northwest, lakes typically form sheltered basins in forested
areas where woodburning emissions and other pollutants collect, often with many
families residing and breathing the bad air in those wooded basins. In the
near-absence of forests in the Dakotas, the lakes don't form such sheltered
areas for collecting polluted air. (See these leading pictures from
tourist-promotion sites for both Dakotas.)
Population density is another determinant of toxins in the air, almost all of which arise from various forms of combustion. In that regard note that population density in the Dakotas is one-sixth as high as in Minnesota (Census Bureau). The dark areas showing Norwegian and Swedish ancestries in the Dakotas show percentages, in thinly-populated areas; that probably makes formation of communities with common ancestries (and therefore long-term continuation of the high-fat Scandinavian diet) less likely in the Dakotas.
Also note that the Dakotas, like Vermont, are landlocked, and are therefore not as subject to high levels of atmospheric mercury (and possibly other toxins) as the coastal states are. Minnesota isn't coastal, but it is home to the most active port on the Great Lakes (Duluth) as well as the Mississippi River port in St. Paul. Over 5 million tons of commodities passed through Twin Cities river terminals in 2010, apparently with most of that activity right in the middle of the city of St. Paul.(http://www.sppa.com/river-shipping-terminals/)
Section 1.2.l Effects of Precipitation:
Fig. 1.7 Average Precipitation Levels in the U.S.
Another environmental
feature that helps keep toxin levels down in the Dakotas is a low level of
precipitation. Precipitation brings toxins in the atmosphere down to the
human-level environment. As this map shows, Minnesota is mostly in the zone of
medium precipitation, and the Dakotas are in the zone of low precipitation.
Maine and the most-populated, high-autism part of Oregon have high precipitation.
Low-precipitation zones also receive more sunshine; greater amounts of
sunshine reduce formation of dioxins, shorten the toxic lives of dioxins that
are present, and enable the body to create vitamin D, thereby promoting immune
function, which is associated with lower levels of autism (see Section 3). Of the ten states on this
map that are mostly low in precipitation (mostly red, brown and/or tan, but excluding
the very exceptional California), every one is below the national median
rate of autism; their average rate is 25% below the national median.
So we have seen that, at the high end of the widely varying rates of breastfeeding in the U.S., the direct association with autism is strong, but it is complicated by
a) effects of varying diets, which in turn affect the levels of toxins in typical breast milk, and also
b) effects of different levels of precipitation, which also greatly influence the levels of toxins in breast milk. It does so principally by affecting amounts of toxins that are deposited on vegetation that is consumed by farm animals whose meat is eaten by childbearing women in the region, as well as by affecting amounts of toxins that end up in lakes and rivers and then come up the food chain into freshwater fish that are eaten.
Section 1.2.m Probable Effect of Low Levels of Breastfeeding: At the low end of the spectrum of varying breastfeeding rates, the association between breastfeeding and autism is not complicated. The seven U.S. states with the lowest rates of breast feeding are all in the bottom third of autism rates in the contiguous U.S. states. (Kentucky, West Virginia, South Carolina, Arkansas, Alabama, Louisiana and Mississippi). (Iowa's reported rates were omitted from this list on the grounds that its data are not comparable with data from the other states, since its four-year trend was completely at odds with the trends in the other 47 states.
1.2.n Breast Feeding in the U.S. Increasing While Mental Disabilities among Males Born have been Increasing
In addition to the increase in toxins in breast milk in recent decades, actual prevalence of breastfeeding has also increased considerably in the U.S. since the 1970's, rising sharply between the early 1970's and early '80's,(A comparison of breast-feeding data from the National Surveys of Family Growth and the Ross Laboratories Mothers Surveys.A S Ryan et al.) then pausing in growth, then continuing to rise substantially during the 1990's and 2000's. (http://www.cdc.gov/breastfeeding/data/NIS_data/index.htm ). During those same decades, mental disability rates among males born during that period increased substantially.(1) There could be a causal connection between the above two increases, given the neurodevelopmental toxins known to be concentrated in most human breast milk in developed countries (especially in the U.S.) in recent decades; this applies especially to dioxins and PBDEs, both of which interfere with testosterone, which is necessary for normal male brain development. Testosterone is also involved in female brain development, but it is clearly far less important than in males; and testosterone in females is obviously not produced in testicles, which are especially vulnerable to effects of toxins. This could help explain why mental disability in females has been able to decline substantially during this same period, along with the major declines in environmental lead and PCBs, while mental disability was rising among males
At this point the breastfeeding promotional efforts of healthcare providers should be diverted to encouraging women to change their dietary habits years before giving birth, and research funds should be devoted to developing improved infant formula that doesn't have the alleged disadvantages of the kinds that are currently available.
Section 1.2.o Another look at Europe: As noted above, Ireland appears to have a very low rate of breast feeding and also low autism prevalence. Norway and Sweden have very high rates of breast feeding, and also high rates of autism. The U.K. is in between in breastfeeding rate (see table below) and also in between in autism rates (Report of UK Task Group on Autism, at http://www.deni.gov.uk/prevalence.pdf , p. 64). (Data don't seem to be readily available for comparing both of these two different kinds of rates for countries other than those four, but any readers are urged to identify to this author any good sources they find for such data.) Ireland's low rate of autism compared with that of either Norway and Sweden can be associated not only with its low prevalence of breastfeeding but also with the probable contents of Irish breast milk compared with the contents of Scandinavian breast milk that is affected by a high-fat diet. As clues to the typical consumption of meat (the other major source of dioxins and mercury in the average mother's diet) for the average Irish, Norwegian or Swedish citizen,
a) there are over twice as many vegetarian restaurants in Ireland per capita as in either Norway or Sweden (www.happycow.com and www.worldatlas.com). This difference is not apparently due to greater ability of Irish people to afford the expense of eating out, since per capita income on a "purchasing power parity basis" is essentially identical between Ireland and Sweden, and oil-wealthy Norway is substantially better off than both; ("The World Fact Book" at www.cia.gov).
b) if one particular food is an unusually large part of a people's diet, other kinds of foods would correspondingly be consumed in smaller quantities. Potatoes were such an important part of the Irish diet, at least in the 19th century (and probably continuing to a great extent today), that a blight affecting only that one crop caused a million to die from famine and a million or more to emigrate from Ireland. More potatoes in the diet probably means less of the dioxin-containing meat, fish and dairy products.
So we see that differences of interest between low-autism Ireland and high-autism Norway and Sweden are both rates of breastfeeding and the differing probable contents of each liter of breast milk. There are, again, other factors involved in the variation in autism rates among these countries, including (a) greatly reduced beneficial effects of sunlight in Norway and Sweden, and (b) probably greater indoor pollution in Scandinavian countries where buildings and residences are likely to be tightly sealed against the cold, therefore possibly less well ventilated, providing greater exposure to toxins in indoor air.
Section 1.2.p Possible Effects of International Variations in Breast Feeding Levels Over Lifetimes
Human breast milk is known to have several ingredients that are especially nutritious for human infants, and various alternative milk formulas for infants are considered to have disadvantages by comparison. Two generations ago the case would have been overwhelming in favor of extended, exclusive breastfeeding. But the world has changed since then, and there needs to be a re-examination that considers drawbacks of breastfeeding, as presented in this paper. Apparently many studies have found health benefits in breast feeding, but probably all of those studies compared data for breast-fed children with data for formula-fed children, which seems logical on the surface. However, it may make more sense to look at the overall lifetime effects, as much as possible. One obviously can't do so with any precision, but the following will provide some quick back-of-the-envelope thoughts on the subject:
Among nations, low rates of breastfeeding apparently do not detract from long-term health:
--- As mentioned earlier, Irish
breastfeeding rates are by far
the
lowest in Western Europe and North America. As indicated by other data shown
at an arrow here, exclusive breastfeeding prevalence for the UK is very
unusually low. (The previously-quoted British rates were not for exclusive
breastfeeding, which is more meaningful for determining total levels of toxins
transmitted in breast milk.) (OECD chart inserted here was found in
publication, "Australian
National Breastfeeding Strategy 2010 – 2015")
--- Since practices like breast feeding are probably connected with culture, handed down through the generations, it is probably safe to assume that breastfeeding rates in Ireland, Italy, and the U.K. were also low during the period when infants were being fed whose eventual deaths have been forming the current life expectancy data.
--- If formula feeding of infants were to be a long-term disadvantage to health, the average life spans of Irish and U.K. citizens would be expected to be below average. But that is not at all the case. According to the U.S. Central Intelligence Agency's "World Fact Book", the "life expectancies at birth" for the U.K. and Ireland are average to above average compared with the other medium and larger Western European countries. Also, those two countries' life expectancies are significantly longer than that for the U.S. In that regard, note that the U.S. expenditure on health care is the highest in the world per capita ("OECD Report Finds U.S. Pays More By Far For Health Care", Kaiser Health News, November 23, 2011).

According to what seems to be the best available source of such information, the rates of breastfeeding for Poland and the Czech Republic are extremely low (see the bottom two lines on this chart). Comparison with Figure 1.4 will reveal that these two countries' breastfeeding rates are very low by almost any international comparison. (This particular chart shows the six countries of Slavic ethnicity that form a cluster in the same general region of Northeastern Europe.) It is interesting to note that Poland and the Czech Republic have life expectancies of 76.1 and 77.2, which are both substantially longer than those of three of the four much-higher-breastfeeding countries in their regional and ethnic grouping (at 66.3, 68.6, 71.2 for Russia, Ukraine and Belarus) (The World Factbook of the CIA, 2012 data). Only Slovakia, at 75.8, is even close in lifespan to the low-breastfeeding countries.
Life expectancy comparisons are confused by the health-damaging effects of alcoholism in Russia and Poland (see
blog exchange at http://www.polishforums.com/society-culture-38/alcohol-problems-polish-people-3868/) and probably to an extent in the other countries also. But there are good reasons why lack of breastfeeding could have been especially beneficial for infants whose lifetimes figure into this chart: Women living in these war-ravaged countries during the 1940's would have been exposed to considerable dioxins in the environment (keep in mind that dioxins are mainly a product of combustion), so typical breast milk in the region would have been especially high in toxins during the mid-century. The especially high dioxin buildup initiated in infants at that time by breastfeeding in this region could have contributed to the early deaths of many of those people, resulting in shorter lives for breastfed people that this chart (combined with the other data) seems to indicate. (Keep in mind that dioxins are either a "probable" or a "known" cause of cancer, depending on which government agency is speaking.)
<<<check the varying war effects in these countries, esp Slovakia>>
But one should not think that only war-ravaged areas expose women to high levels of toxins in the environment. Bear in mind that (1) general levels of dioxins in the environment increased greatly into the late 20th Century in industrial countries, (2) at least some very important varieties of dioxins as well as other environmental toxins continue to increase greatly in the U.S. environment, (3) some areas are especially high in toxin levels <<itemize a few -- paper mills, airports, within 1000 ft/?yards?meters of thruway?)>>, and (4) foods that are widely eaten (especially meat, dairy products, fish, and high-animal-fat products) can contribute heavily to a woman's body burden of dioxins and mercury). The typical Russian diet, high in animal fat, would have contributed to dioxin accumulation in breast milk, in turn probably contributing to average eventual lifespans of only 66.5 years.
In any case, at minimum there appears to be no reason to believe that people suffer significant long-term ill-health effects from low rates of breastfeeding.
Section 1.2.q Review of Some Pros and Cons of Breastfeeding in a 21st Century Industrialized Country, by Women Who have been Eating a Typical Diet: There are good reasons to look into the fact that high rates of autism in certain countries and U.S. states coincide with unusually high rates of breastfeeding in those same countries and states. The uniformly low rates of autism in the U.S. states with the lowest rates of breastfeeding should add weight to the need for a serious re-examination of the widespread promotion of breastfeeding. The higher rate of autism in the white ethnic group, compared with lower rates of autism that are either certainly lower or probably lower in breastfeeding rates, adds still more reason to doubt the desirability of general breastfeeding promotion. All of those geographical, national and ethnic data would be enough by themselves to raise a major red flag. The logical next step is to see if there is scientific evidence showing that contents of breast milk are capable of causing harm to neurological development. See the considerable content earlier in this paper providing exactly that, as regards breast milk in current, more polluted times. And then look closely at the history of the recent decades concerning changes in rates of breastfeeding and rates of autism. No doubt to everyone's surprise by now, the paths of the two rates have tracked very closely <<with the autism lagging behind the rise in breastfeeding by several years?>>. The only conspicuous exception to the tandem rises of the two rates is the case of the U.K.; in that case, breastfeeding did not rise significantly, and autism also did not rise significantly.
One of the various studies finding health benefits in breastfeeding points to the significantly lower rates of colds, cases of diarrhea, ear infections, and doctor visits among infants that are breast fed. And they point out that health care providers should therefore have an interest in encouraging breast feeding, which they clearly do. If the burdens of dioxins, mercury and PBDEs in contemporary women's bodies were the same as they were in the middle of the 20th century, such promotion would be beneficial to infants. But they aren't, and it isn't.
Many women probably tend to think that, since their foremothers may have breastfed for long periods and their children turned out well, and since breastfeeding is widely encouraged, then that must mean that breast feeding is risk-free. But high levels of dioxins, mercury, and PBDEs in the environment, and therefore in breast milk, are a relatively recent development. Researchers cite various studies suggesting that rates of dioxin deposition in the environment increased more than 10-fold between the 1930's and the 1960's (Regulatory Toxicology and Pharmacology, 37 (2003) 202 217 Dioxin risks in perspective: past, present, and future Hays and Aylward at http://acdrupal.evergreen.edu/envirohealth/system/files/Dioxin+risks+in+perspective.pdf). Bear in mind that dioxins are essentially a product of many typical forms of combustion, requiring presence of a source of chlorine as part of the burning, such as is included in the plastics waste that skyrocketed in the U.S. environment in the mid- and late-twentieth century. Mercury is released by combustion of mercury-containing materials, especially ones such as in coal, which has been increasing rapidly with growing populations and industrialization in various parts of the world; since airborne mercury drifts around the globe, considerable emissions from Asia's rapidly-expanding, polluting industries, and from ships going back and forth, are in the U.S. air supply and in the water habitat of fish. PBDE's are something new in recent decades. All of the above mean that breast milk today is very different from that of earlier periods. New releases of dioxins by U.S. industry have declined recently, but other sources that closely affect humans (especially diesel emissions) have increased greatly at the same time. And dioxin levels in soil (partly ingested by farm animals, and often ingested by infants) almost certainly continue to increase due to the extremely long lives of dioxins in soil, even though they are increasing less rapidly than in earlier decades. A long-term, mostly-vegetarian diet is apparently the only way for a woman to avoid major buildup of dioxins and mercury within her body. Minimizing breathing of air in the vicinity of electronic devices (especially where ventilation isn't good) might be the only way to avoid buildup of PBDEs.
As was pointed out with several international examples earlier, countries in which breastfeeding is relatively rare have life expectancies at least as long as countries in which breastfeeding is more common. But the case against claims of health benefits from breastfeeding is much stronger than that. The people whose lifetimes have been forming the basis for current average life expectancies were breastfed at a time before environmental levels of dioxins and other toxins had come anywhere near their present levels. Dioxins, which accumulate in the body over the years, are also very much associated with cancer and other usually-adult diseases (see www.epa.gov/dioxin/). So present day breastfeeding, by mothers with body burdens of dioxins that are typical in modern industrial countries, would be getting infants off to a start in accumulation of toxins that could lead to cancer or other diseases decades later. (Remember from Section 1.2.d the quote from the National Academy of Sciences about a breastfed baby during its first year receiving 87 times the average adult dosage of dioxins.) When looking at information promoting breastfeeding, check carefully to see how far into adulthood their comparison studies go; if you find any that go past childhood, please inform this author (at dm@pollutionaction.org). National life expectancy comparisons that merely cast serious doubt about long-term benefits of breastfeeding don't fully apply currently, since they don't reflect the greatly increased typical present-day levels of persistent neurological toxins in breast milk.. It would only be prudent to assume that the current increased level of toxins, when combined with additional, accumulating exposures to toxins later in life, would have long-term effects of kinds that scientific studies have found to be caused by those toxins. That should probably tip the balance of the assessment of long-term physical health effects of most current breastfeeding in industrial countries over to negative. Apparent neurological effects of breastfeeding, greatly increased autism and unusually large numbers of people with non-traditional sexual preferences, have already been presented.
1.2.r Breast Feeding in the U.S. Increasing While Mental Disabilities among Males Born have been Increasing
In addition to the increase in toxins in breast milk in recent decades, actual prevalence of breastfeeding has also increased considerably in the U.S. since the 1970's, rising sharply between the early 1970's and early '80's,(A comparison of breast-feeding data from the National Surveys of Family Growth and the Ross Laboratories Mothers Surveys.A S Ryan et al.) then pausing in growth, then continuing to rise substantially during the 1990's and 2000's. (http://www.cdc.gov/breastfeeding/data/NIS_data/index.htm ). During those same decades, mental disability rates among males born during that period increased substantially.(1) There could be a causal connection between the above two increases, given the neurodevelopmental toxins known to be concentrated in most human breast milk in developed countries (especially in the U.S.) in recent decades; this applies especially to dioxins and PBDEs, both of which interfere with testosterone, which is necessary for normal male brain development. Testosterone is also involved in female brain development, but it is clearly far less important than in males; and testosterone in females is obviously not produced in testicles, which are especially vulnerable to effects of toxins. This could help explain why mental disability in females has been able to decline substantially during this same period, along with the major declines in environmental lead and PCBs, while mental disability was rising among males
At this point the breastfeeding promotional efforts of healthcare providers should be diverted to encouraging women to change their dietary habits years before giving birth, and research funds should be devoted to developing improved infant formula that doesn't have the alleged disadvantages of the kinds that are currently available.
1.3 Harmfulness of Lead in even the Smallest Amount, and Terminology related to Mental Retardation
In addition to what is widely known about harmfulness of lead to mental development, we add the following from the EPA's website: "Lead is the only chemical treated as a non-threshold non-carcinogen. That is, adverse health effects can occur at any level of exposure. A great deal of information on the health effects of lead has been obtained through decades of medical observation and scientific research…. It appears that some of these effects, particularly changes in …. aspects of children’s neurobehavioral development, may occur at blood lead levels so low as to be essentially without a threshold…." (19) (emphasis added)
Mention should be made here of the different terms that are used
to mean very much the same thing. "Mental retardation" has for many
people become an overly negative, pessimistic term; according
to Wikipedia, "over 100 ... organizations are striving to eliminate the
use of the "r-word" (analogous to the "n-word") in
everyday conversation." Some government agencies
now instead use subdued terms in describing the effects of lead and other
toxins, such as "causes lower IQ" or "changes neurobehavioral
development" or "causes developmental delay." But such terms
tend to mask the life-impairing seriousness of the toxins to which infants are
often exposed. It should be born in mind that a specific "lower IQ"
(below a score of 70) has long been the standard basis for determining mental
retardation, that "delayed development"
in actuality is normally permanent rather than delayed, and that "changes
in neurobehavioral development” is an abstract way to tell what is probably
happening when infants' brains are becoming those of autistic children or
delinquents or are losing the ability to focus attention. <<?Medline Plus, a medical encyclopedia published by the
NIH, comes a little closer to words that acknowledge the gravity of lead's
hazards in saying that it "can affect children's developing nerves
and brains. The younger the child, the more harmful lead can be. Unborn
children are the most vulnerable."
Figure 2a1
As shown in this chart, there has been a huge drop in what is considered acceptable blood levels of lead in children. Various studies have determined that each 10 ug/dl in lead level makes a difference of between 3 and 5.5 points in a child's IQ. So lead levels that were considered acceptable in the 1960's could easily have been causing 15 to 27 points in lower IQ for each affected child. Bearing in mind that a score of 100 is in the exact center of the IQ range and below 70 is considered to be mentally retarded, that means that lead exposure that was considered acceptable as of the 1960's could have been lowering the IQs of many children from middle-range to that of retardation. So a large part of the mental retardation of earlier decades may have resulted essentially from lead.
It is probable that the major decline in mental disability among females that occurred in the last generation or so resulted largely from the huge decline in lead levels that took place. Reduced effects of lead in males may have been cancelled out by increases in effects of other environmental toxins that took place over recent decades, toxins which affect males specifically (including the ones mentioned in this paper that are known to cause testicular atrophy).
Fig. 2a2 (from http://www.epa.gov/air/airtrends/lead.html) Fig. 2a3


1.4 Particulate Matter (PM) and Diesel Exhaust
The EPA oversees substantial research on "particulate matter", but typically only publishes environmental pollution data for "diesel particulate matter", as in the EPA's NATA 1999 air toxics assessment. That phrase was replaced in the NATA 2002 assessment with "diesel engine emissions". There is considerable overlap in what is encompassed in the meanings of the three above phrases, as well as substantial differences. But particulate matter from diesel emissions seems to be the specific kind of PM that the EPA considers to be of the greatest significance.
In an EPA document, the authors pointed out findings of a study suggesting that "…the central nervous system is a potentially important toxicologic target of PM2.5 (very tiny particles of the kind predominant in diesel emissions)… In support of this significant result, studies of mice chronically exposed to ambient PM2.5 documented loss of brain neurons (Veronesi et al. 2005) and changes in gene expression in the brain….."(20) (italics added) In a report about work at the University of Rochester's Environmental Sciences Center, findings are stated that "inhaled ultrafine particles can reach the central nervous system" and can do so efficiently.(23)
In addition to complete particles reaching the nervous system, organic compounds (which include dioxins and PAHs) adsorbed onto particles can be freed from the particles and "rapidly absorbed into the bloodstream." (24) (parenthetical expression added) The EPA document on PM Centers cited earlier in this section refers to "a number of PM Center studies (providing) a strong evidentiary basis for oxidative damage as a general toxicologic mechanism of PM injury." Metals in PM were found to play a role in formation of "reactive oxygen species," which are extremely reactive molecules and ions that can harm cells. If words like "oxidative" and "reactive oxygen" are not familiar terminology to the reader, bear in mind that oxidation damages or destroys matter, sometimes quickly (as in burning) and sometimes slowly, as with rust.
Aside from evidence about general neurological harm resulting from oxidative damage, a team of scientists studying the connection between vehicular exhaust and autism referred in 2011 to "emerging evidence that oxidative stress and inflammation are also involved in the pathogenesis of autism."(24b)
Notice that most of the above indications of harm that can be caused by PM refer to effects on tissues and brains in general, regardless of age. The specially great vulnerability of developing brains should be considered in light of the statement by the NIH (quoted in Section 1.1) about the "greatest risk … when organ and neural systems are developing." The 2011 study quoted in the previous paragraph states that "Diesel exhaust particles present in traffic-related pollution have been shown to have endocrine-disrupting activity and to transplacentally affect sexual differentiation and alter cognitive function in mice ." (24b) (emphasis added). Another relevant experiment was conducted on male rats over a three-month period beginning at birth, in which it was found that diesel exhaust was responsible for "disrupting the endocrine system".(25b) Also, scientists replicated lungs of infants to compare with replicated lungs of adults, tested both for particle deposition after exposure to particles, and concluded that "tracheobronchial dose on a per kg body mass basis……may be more than six times higher in the resting newborn than in the resting adult."(25)
In Section 4.4 of the EPA's 2002 Health Assessment Document for Diesel Engine Exhaust, it is pointed out that, "Extensive studies with salmonella have unequivocally demonstrated mutagenic activity…. Several of the chemicals found in diesel emissions possess mutagenic activity in a variety of genetic assays." That same document points out that approximately 80%-95% of the mass of particles in diesel exhaust are in the size range from 0.05-1.0 microns which, "due to their small size, can effectively reach the lower portions of the respiratory tract."(58)
The fact that diesel emissions are a major source of dioxins ties in with the previously-mentioned effects observed to result from PM and diesel emissions: altered cognitive function, loss of brain neurons, and changes in gene expression. (The action of dioxins as endocrine disruptors, probably resulting in interference with normal brain development, was discussed in Sections 1.2.a and 1.2.b.)
Although PM is the component of diesel exhaust that probably receives the most attention, harm to the developing brain is seen to result also from other diesel emission components that are sometimes studied separately, including PAHs.(24c) "Specific pollutants, including (various components of diesel exhaust), have also been associated with significant differences in biparietal diameter and head circumference measured both during pregnancy and at birth (Hansen et al. 2008; Vassilev et al. 2001). Maternal exposure to polycyclic aromatic hydrocarbons (PAHs) during pregnancy has been associated with impaired cortical (referring to the outer part of the brain) function …." 24b (parenthetical expressions and emphasis added) Regarding how best to protect infants against the effects of diesel emissions, it is noteworthy that the above researchers found that, "Because these effects were not inhibited by filtration, the gaseous phase of the (diesel) exhaust appears more responsible than particulate matter for disrupting the endocrine system." However, later in that same EPA document (section 5.3) it is stated that "When adsorbed onto diesel particles, the gases and vapors can be transported and deposited deeper into the lungs, and because they are more concentrated on the particle surface, the resultant cytotoxic (harmful to cells) effects or physiological responses may be enhanced." So there appears to be some question regarding which of the specific components of diesel emissions are likely to cause the most serious damage to neurological development.
Diesel emissions from trucks and trains are especially likely to be harmful because they are released close to ground level, from large numbers of exhaust pipes that are travelling thousands of miles on roads and tracks that are widely distributed within populated areas. Those emissions quickly and directly reach the air breathed by many infants and pregnant women, and their particulate matter lands on surfaces crawled on by many infants, as well as on objects handled, and on soil that could then be ingested by infants. A study of effects of proximity to California freeways (published in 2011) found a considerably elevated percentage of cases of autism among infants residing within about 1000 feet of a freeway. 24b) That study was probably mainly finding the effects of diesel emissions from passing trucks, as indicated by the following: According to EPA data for the year 2000, total dioxin toxic equivalency produced by on-road diesel emissions in the U.S. was about 17 times as high as the total produced by on-road unleaded gas fuel combustion emissions (Figure 1-8 in EPA/600/P-03/002F November 2006 An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000)
Diesel emissions have been found in a study to be harmful to the endocrine output of male test animals. "Sperm production and hyaluronidase activity, one of the biochemical markers for testicular toxicity (43-45), were reduced in the diesel exhaust-exposed rats…. These elements indicate that testicular function was suppressed by the inhalation of diesel exhaust. …the male reproductive system may be particularly susceptible to toxic insult during the gestation period, as has been observed….in various studies." (25b) "Inhalation of Diesel Engine Exhaust Affects Spermatogenesis in Growing Male Rats," N Watanabe and Y Oonuki, Department of Environmental Health, Tokyo Metropolitan Research Laboratory of Public Health, Tokyo, Japan. nobuew@tokyo-eiken.go.jp. Environmental Health Perspectives, Vol. 107, No. 7, accessed at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566672/ ) It should be noted that, although the level of the test animals' exposure in this experiment was well above the average urban U.S. diesel pollution levels, that exposure was for only a total of 30 hours per week, and it didn't begin until after birth. In that regard, remember from a study quoted previously that diesel emissions have been shown to act transplacentally (24b), and remember that the brain is going through very important development before birth. So the exposure to diesel emissions applied in this study probably came after the equivalent period when harmful exposure to diesel emissions in a typical urban environment would have already been well underway, but this abbreviated exposure nevertheless had a significant effect.
The "bunker" type of fuel that is used in ocean-going ships and for heating in some large urban buildings is an atypical form of diesel fuel. It is a tar-like product consisting of the residual that remains after distillates are extracted from crude oil in the process of making other kinds of fuel, with many toxic components concentrated in that residual. Most people are surprised to learn that the EPA has calculated that many thousands of deaths occur in North America every year as a result of marine diesel emissions.(d65), although substantial death rates have also been attributed to land-based diesel emissions (per EPA announcements). An EPA document regarding diesel pollution from ocean shipping points out that the PM contained in marine diesel emissions includes mercury, lead, and dioxin, as well as arsenic and other metals. (a9). It also points out that "Marine diesel engine emissions consist of a higher fraction of ….. metallic ash (approximately 7-11%) than (is) typically found in land-based engines".(a10) Another authoritative source places the fraction of metallic ash in diesel emissions of PM 2.5 and PM 0.1 (the deepest-penetrating categories of PM) at between 17% and 25%.(a17) The higher proportion of metallic ash in marine diesel emissions is important not only because of the known toxicity of some of the metals but also because formation of dioxins during combustion is promoted by metals' acting as catalysts during the combustion.(EPA/600/P-03/002F November 2006, p. 2-2) Between that and the presence of sodium chloride in sea air (as a source of the chlorine needed to form dioxins), marine diesel emissions may be substantially higher in dioxins than is average for other diesel engine exhaust, and they almost certainly contain a higher proportion of mercury and lead.
Summarizing: Particulate matter and diesel emissions can be generally harmful to central nervous systems. Infants can receive dosages that are effectively several times higher than adults. Infants can receive those effectively very high dosages at the worst possible time, when their brains are developing and before their defense mechanisms have matured..
1.5 Mercury
An EPA web page on mercury points out the following: "for fetuses, infants, and children, the primary health effect of methylmercury is impaired neurological development."(37) "Methylmercury exposure adversely affects a number of cellular events in the developing brain both in utero and post-natally.(38, p. 49) …There is an extremely high level of scientific certainty that methylmercury causes these changes (abnormalities in the human brain)." (p. 51) The only question is when the effect is most likely to occur: "it is not possible to precisely identify the period of development during which mercury is likely to damage the nervous system of the developing fetus or growing child"(39). One study of hazardous air pollutants found a moderate association of autism with estimated airborne metal levels at birth, most notably mercury, cadmium, and nickel. (40)
Mercury to which children (and all of us) are exposed comes only partly from nearby sources, since airborne mercury can stay in the air for a year and travel thousands of miles.(41) What isn't breathed in by humans and animals is deposited to a great extent onto trees and plant life or is taken in through the stomata of plants, or falls onto the soil from where it enters plants' roots, thereby entering the food chain. But absorption by marine plant life, which is then eaten by fish, which in turn are eaten by other fish, is normally considered to be the largest primary avenue for mercury into human bloodstreams. This effect of increasing mercury at higher levels in the food chain usually has greater impact in freshwater fish than saltwater fish.
Exposure of infants and child-bearing women to mercury varies tremendously, and is a serious concern. Among children aged 3-6, the 5% who consume the most fish and shellfish receive ten times more exposure to mercury from the fish than does the average child. Among women of child-bearing ages, the 1% who consume the most fish receive over thirty times as much mercury as the average. 5% of children have methylmercury exposures from fish/shellfish two-to-three times the EPA's recommended safe maximum amount (RfD). (EPA-452/R-97-006, December 1997, Mercury Study Report to Congress. Volume IV: An Assessment of Exposure to Mercury in the United States, Tables 4-70, 71 &72, and p. ES-3) However, the benefits of Omega 3 fatty acids in fish to mental development are also believed to be significant. A 2005 research study found that infant "cognition" at six months of age was normally lower when mothers had higher levels of mercury, but it was higher with mothers who ate more than average amounts of fish, which caused the authors to recommend that mothers eat ample amounts of specific species of fish that are known to be low in mercury. (Maternal Fish Consumption, Hair Mercury, and Infant Cognition in a U.S. Cohort, Emily Oken et. al., Environmental Health Perspectives, Oct. 2005)
Wildfires and residential wood burning cause deposited or absorbed mercury to re-suspend into the air, and this re-suspension takes place in concentrated form; the re-suspension during fires is likely to be from the heated soil (including deposited, decayed vegetation) as well as from living vegetation (41b). An environmental toxicologist at the Oregon Department of Environmental Quality was quoted in The Oregonian as saying that he "could tell when wildfires were burning by looking at data from mercury monitors. The fires send mercury levels three or four times higher."(41c) According to the EPA, 50 tons of mercury were emitted from burning of coal in U.S. power plants in 1999, even after considerable reductions took effect as required by the Clean Air Act of 1990. (http://www.epa.gov/mercury/control_emissions/index.htm )
1.6.a Pesticides: In a study published in 2007 by researchers with the state of California, of children who went through gestation in the vicinity of where organochlorine pesticides (principally dicofol and endosulfan) were applied agriculturally, it was found that eight subjects had ASD where the normal expected number of cases would have been 1.8. "Risk for ASD was consistently associated with residential proximity to organochlorine pesticide applications occurring around the period of CNS embryogenesis (early development of the central nervous system); this association appeared to increase with dose and was attenuated with increasing distance of residence from the field site."(In Environmental Health Perspectives, of the NIH, found at http://ehp03.niehs.nih.gov/article/fetchArticle.action?articleURI=info:doi/10.1289/ehp.10168 : "Maternal Residence Near Agricultural Pesticide Applications and Autism Spectrum Disorders among Children in the California Central Valley", Eric M. Roberts et al.) The EPA banned the use of endosulfan and dicofol in 2010 and 2011, after both had been in use since the 1950's.
Chlorpyrifos is the first pesticide mentioned in a statement about insecticides that "have long predominated for insect control on lawns, shade trees and shrubs, and nurseries." (Classes of Pesticides Used in Landscape/Nursery Pest Management, Whitney Cranshaw, Colorado State Univ., accessed Jan. 2012 at http://www.entomology.umn.edu/cues/Web/042ClassesOfPesticides.pdf) "Chorpyrifos exposure was linked to changes in social behavior and brain development as well as developmental delays in young laboratory animals.…. Researchers studied the blood of women who were exposed to chlorpyrifos and the blood of their children from birth for three years. Children who had chlorpyrifos in their blood had more developmental delays and disorders than children who did not have chlorpyrifos in their blood. Exposed children also had more attention deficit disorders and hyperactivity disorders." (Chlorpyrifos – General Fact Sheet National Pesticide Information Center, Oregon State University in cooperation with US EPA) Note that the EPA seems to use the term "developmental delay" the way "mental retardation" would have been used in earlier, less-sensitive times. It is interesting to note that (in a European study) exposure of rat fetuses to low dosages of chlorpyrifos during gestation "did not induce large immediate effects on brain development [49], but ….did cause deficits in brain cell numbers …(and capabilities)... which emerged in adolescence and continued into adulthood." (emphasis and parenthetical expression added) (Potential developmental neurotoxicity of pesticides used in Europe Bjørling-Poulsen et al; Environ Health. 2008; 7: 50.Published online 2008 October 22.) Studies that claim to find no decline in mental or other health in children exposed to various environmental toxins (such as those typically included in breast milk) may not continue long enough to detect long-term consequences, including cancer as well as neurological effects such as mentioned above.
Note that the above experiment was not unusual in finding harmful effects in offspring even when dosages were low enough so as not to be harmful to the adults. "Studies in laboratory animals support the notion that a wide range of industrial chemicals can cause developmental neurotoxicity even at low doses that are not harmful to mature animals." (Bjørling-Poulsen et al. )
"Many pesticides target the nervous system of insect pests. Because of the similarity of neurochemical processes, these compounds are also likely to be neurotoxic to humans…. Some 60% of all herbicides… have been reported to interfere with thyroid function…. A key concern with thyroid inhibitors is that impaired thyroid function may alter hormone-mediated events during development, leading to permanent alterations in brain morphology and function…. Even within the normal range, a relatively slight reduction of the concentration of maternal thyroid hormones during pregnancy can lead to intelligence deficits in the children."(Bjørling-Poulsen et al. )
"Vinclozolin, a fungicide used on many types of fruits and vegetables, is a potent anti-androgen…. Many thiocarbamide and sulfonamide-based pesticides such as ethylenethiourea (22) and linuron (23) have anti-thyroid effects…." (Gray LE Jr, Ostby JS, Kelce W. Antiandrogenic effects of the fungicide vinclozolin on sex
differentiation of the rat. Toxicol AppI Pharmacol (in press). Remember from Section 1.2.b.1 the finding from one study that "a lack or excess of thyroid hormone arising at specific stages can cause irreversible neurological damage."
"Many of the persistent organochlorine pesticides …have been identified as endocrine disruptors…. pups (exposed to some of these chemicals) were impaired on both learning and retention of active avoidance tasks."(Cognitive Effects of Endocrine-Disrupting Chemicals in Animals, Susan L. Schantz and John J. Widholm, Department of Veterinary Biosciences and Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, Illinois, in Environ Health Perspect 109:1197–1206 (2001). [Online 14 November 2001] Found at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240501/pdf/ehp0109-001197.pdf) The pesticides procymidone and vinclozolin are anti-androgens. "A number of organochlorine pesticides, including Kepone, methoxychlor, and zearalenone, have been shown to masculinize female rats. Tamoxifen demasculinizes male rats." (Environmental Endocrine Disruption: An Effects Assessment and Analysis, by Thomas Crisp et al, EPA, in Environmental Health Perspectives, Vol. 106, Feb. 1998, Supplement, pp. 24, 29 )
The EPA conducted a study assessing data availability on close to 3,000 chemicals that the United States produces or imports at more than 1 million pounds per year and concluded that only 23% of those chemicals had been tested for reproductive and developmental toxicity. Test data were considered available if any studies relevant to reproductive and developmental toxicity were located. (Scientific Frontiers in Developmental Toxicology and Risk Assessment (2000) Commission on Life Sciences, National Academy of Science, National Academies Press, p. 24) Note that this small percentage of any kind of developmental testing applied to the highest-volume chemicals in the U.S.; nearly 100,000 different chemicals are currently in commercial or industrial use in the U.S. Even if testing is performed, one may wonder whether the testing is normally sufficient to find out about all or most of the likely harmful effects. Note that, in a study quoted earlier (Watanabe et al.), it was difficult to detect the testicular toxicity of diesel exhaust, since "by external appearance, the testes from the control and exhaust-exposed animals were indistinguishable." Also, if early exposure to pesticides affects mental development in ways that would handicap a human in modern society, those effects would often not show up in typical testing of laboratory animals. Possible examples would be ability to concentrate on school work (think ADHD), to speak and act normally and interact normally with fellow humans (think autism), to perform mathematical reasoning, or to conform to society's standard sexual orientation. Effects similar to most of the above have been found in various pesticides that have been in use in the U.S., but nobody knows how many such effects have not been found in pesticides due to lack of testing or failure of tests on animals to detect all possible significant effects on humans. Note the example in the first paragraph of this section about two pesticides in use in the U.S. for over half a century before they were banned, following soon after a careful study (finally) of their apparent effects.
1.6.b DEHP: A web page of the FDA * *(http://www.fda.gov/downloads/MedicalDevices/DeviceRegulationandGuidance/GuidanceDocuments/UCM080457.pdf) points out that DEHP (a phthalate, found in many plastics) has been shown in experiments with animals to cause testicular atrophy. The special significance of testicular atrophy in a discussion of neurological impairment can be seen in Section 1.2.b of this paper, which explains the importance of testosterone in development of the infant brain. A web page of the U.S. Agency for Toxic Substances and Disease Registry points out that animal studies suggest that young males are even "more susceptible than adults to adverse effects on the sex organs."
It should be noted that DEHP has been widely used as a plasticizer for manufacturing many plastic products with which infants can come into contact, including flexible toys, floor tiles, table cloths, furniture and auto upholstery, baby pants, shoes, rainwear, and food and beverage containers. (from website of the ATSDR at http://www.atsdr.cdc.gov/toxfaqs/tf.asp?id=377&tid=65 ) It has apparently been banned in children's products as of 2008, but there are probably many still in use. An especially likely avenue for exposure of infants is via runoff of DEHP from shower curtains into tubs in which infants will later be bathed, with soapy water being a likely medium for lifting and re-suspending the dried DEHP residue and helping it soak in through the skin, especially into the very exposed male scrotum and then into the testicles.
Figure 2a4
The ATSDR is particularly concerned about infants' chewing on plastic objects not designed for that purpose. According to a small poll taken by the author of this paper, that sort of thing is extremely widespread. But the ATSDR points out that even skin contact with plastics can be a source of exposure to DEHP. The agency indicates that other likely sources of low-level exposure include packaging "especially of fatty foods like milk products, fish or seafood, and oils." (Fatty foods are of special concern, since fat helps the DEHP to dissolve and transfer.)
Since mere skin contact with plastics can be a source of exposure to DEHP, consider how much greater would be the exposure of an infant in a tub to water containing runoff from DEHP-containing shower curtains, or bromine or PCBs in the water supply, or possible toxins in cleaning solutions.
"… phthalates in pregnant women’s urine was linked to subtle, but specific, genital changes in their male infants – … incomplete descent of testes and a smaller scrotum and penis (Swan et al. 2005)."(http://e.hormone.tulane.edu/learning/human-effects.html , Tulane University: Endocrine Disruption Tutorial)
<<insert re PCP, drawing from Indiana secn, >>
1.7.1 Dioxin-like PBDE Levels Rapidly Increasing in Breast Milk, and especially High in the U.S., and Affecting Males especially: PBDEs are chemicals whose main environmental properties and mechanisms of toxicity are similar to those of the structurally-related PCBs and dioxins.(Rev Environ Contam Toxicol. 1995;141:1-26. Polybrominated biphenyl and diphenylether flame retardants: analysis, toxicity, and environmental occurrence. Pijnenburg AM, Everts JW, de Boer J, Boon JP. National Institute for Coastal and Marine Management (RIKZ), Ministry of Transport, Public Works and Water Management, The Hague, The Netherlands.) According to the Swedish National Food Administration, "the critical effects of PentaBDEs are those on neurobehavioural development … and, at somewhat higher dose, thyroid hormone levels in rats and mice…." (Toxic effects of brominated flame retardants in ... [Environ Int. 2003] - PubMed - NCBI http://www.ncbi.nlm.nih.gov/pubmed). PBDEs are also likely to be endocrine disruptors. (Envir. Health Perspectives, May, 2000: The PBDEs: An Emerging Environmental Challenge and Another Reason for Breast-Milk Monitoring Programs Kim Hooper1, Thomas A. McDonald2), Bear in mind the importance of testosterone to development of the brain when reading the following quote: "…most PBDEs have antiandrogenic activity…. Some PBDEs and their metabolites (e.g. OH-BDE-47) have been found to inhibit activity of CYP17, a key enzyme in the synthesis of testosterone…."(DEVELOPMENTAL NEUROTOXICITY OF POLYBROMINATED DIPHENYL ETHER (PBDE) FLAME RETARDANTS Costa and Giordano 2008 Neurotoxicology National Center for Biotechnology Information, U.S. National Library of Medicine, Bethesda, MD, 20894USA) "Many experimental studies consistently reported neurotoxic effects following perinatal exposure to PBDEs."(Polychlorinated Biphenyls (PCBs) and polybrominated diphenhyl ethers (PBDEs) in milk from Italian women living in Rome and Venice", Ingelido et al., Chemosphere, Vo. 67, issue 9, April 2007, obtained from Air Force Institute of Technology, ILL.
PBDEs are used as flame retardants in TV sets, computers, other electronics, some plastics, and foam cushioning (although most use of PBDEs in foam cushioning manufactured in the U.S. was discontinued by 2005). Their use is still permitted in the United States but has been banned in some European countries. A study of 47 breast milk samples in Texas found PBDE levels similar to levels found in blood and fat tissue from California and Indiana, which were ten to one hundred times higher than levels found in humans in Europe. (Environ Health Perspect. 2003 Nov;111(14):1723-9. Polybrominated diphenyl ethers (PBDEs) in U.S. mothers' milk. Schecter A, et al., found at http://www.ncbi.nlm.nih.gov/pubmed/14594622) In 1998, research with archived samples of breast milk in Sweden found that PBDE levels in the milk had been doubling every 5 years over the preceding 25 years, but no one had known about it.(Hooper K, She J 2003. Lessons from the Polybrominated Diphenyl Ethers (PBDEs): Precautionary Principle, Primary Prevention, and the Value of Community-Based Body-Burden Monitoring Using Breast Milk. Environ Health Perspect 111:109-114. http://dx.doi.org/10.1289/ehp.5438 Online: 11 December 2002) It is interesting to note that the Swedish National Food Administration was clearly concerned about the effects of PBDEs on neurological development even though the levels of that chemical in their country were apparently many times lower than those in the U.S. "North America consumes over half of the world's production of polybrominated diphenyl ether (PBDE) flame retardants. About 98% of global demand for the Penta-BDE mixture, the constituents of which are the most bioaccumulative and environmentally widespread, resides here. …." (Environ Int. 2003 Sep;29(6):771-9. Polybrominated diphenyl ether flame retardants in the North American environment. Hale RC, Alaee M, Manchester-Neesvig JB, Stapleton HM, Ikonomou MG. Department of Environmental and Aquatic Animal Health, Virginia Institute of Marine Science, College of William and Mary, Gloucester Point, VA 23062, USA. PubMed – NCBI http://www.ncbi.nlm.nih.gov/pubmed)
Figure 2b
1.7.2 Sun Exposure, which varies greatly by Region, is an important influence on toxicity, and should guide what is avoided by child-bearing women and infants.
1.7.2.a Total Accumulation of toxicity of pollutants is very much affected by sun exposure. At least one of the pollutants that is most implicated in neurological harm, dioxin, can be relatively quickly degraded by sunlight, sometimes in less than a day.((Agency for Toxic Substances and Disease Registry (ATSDR). 1998. Toxicological profile for Chlorinated Dibenzo-p-dioxins (CDDs). Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service, p. 419) That helps explain why levels of neurological impairment are low in the U.S. Southwest, except for autism in certain big California city areas. (See Sections 3.1 and 3.2 about other benefits of sun exposure.) At the other extreme are Maine and Minnesota, with the lowest solar radiation levels of all the contiguous states; those two states have either an extremely high level of mental disability in general (in the case of Maine) or an extremely high level of autism (in the case of Minnesota). In far northern areas there is less industry and traffic and therefore less pollution generated than in more temperate areas; but those limited pollutants, along with toxins blown in from the south, retain much more of their toxicity than in high-solar areas, and that toxicity continues to accumulate in the soil and water through the decades. The EPA quotes two studies estimating the half lives of dioxins on soil to be 9 to 15 years, and half lives of dioxins in soil are estimated to be 25 to 100 years.(EPA/600/P-03/002F November 2006, p. 11-11). In addition to variations in the amount of solar radiation approaching the earth, as shown on this map, the amount that actually reaches ground level can also vary greatly depending on forest cover. That is another area in which Maine has an unusual disadvantage regarding solar benefits, since it is 90% forested.
Fish that eat vegetation or ingest bottom sediment in water that drains from such areas, and/or that eat smaller fish that ingest that vegetation and/or sediment, will "bio-accumulate" higher levels of toxins before (often) being eaten by mothers and infants. It is probably no coincidence that the only state < we have been able to find> that tells residents not to eat freshwater fish caught in that state (with the exception of one specific type of fish) is a New England state.
1.7.2.b Other implications about foods to be avoided by infants and child-bearing women: Farm animals eat not only vegetation that grows in soil that keeps accumulating dioxins but also significant amounts of the increasingly toxic soil itself, sometimes ingesting up to as much as 18% soil in what they eat (Dioxins and Dioxin-like Compounds in the Food Supply: Strategies to Decrease Exposure By Institute of Medicine (U.S.). Committee on the Implications of Dioxin in the Food Supply, National Academy of Sciences. National Academies Press, 2003). The toxins then accumulate in the future food supply of mothers and infants: meat, fat tissue that becomes an ingredient of processed foods, and cheese, butter, and other dairy products. Vegetables growing in dioxin-containing soil can absorb endocrine disruptors from that soil; in one experiment, carrots grown in soil to which dioxin had been added increased their dioxin content by over 800%.(Agency for Toxic Substances and Disease Registry (ATSDR). 1998. Toxicological profile for Chlorinated Dibenzo-p-dioxins (CDDs). Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service, p. 421) Potatoes, beets, and other root and tuber crops could be expected to absorb dioxins from soil in which they grow. The green-living advice common in recent years, about buying locally-grown foods, should probably not be heeded when purchasing food for infants and child-bearing women living in the lowest-solar zones on the above map. Likewise, vegetables grown in one's own backyard garden could be hazardous if the home is near a major throughway, railroad, or port, or downwind from an industrial source of dioxin-containing emissions, or near a hazardous waste site.
1.7.2.c Non-foods to be especially avoided in northern areas and high-pollution areas: In addition to dioxins from foods, infants very often ingest soil and dust which contain dioxins. Section 2.4 deals with that topic, pointing out that researchers have found dioxins in soil to be far higher than expected, and levels of dioxins in soil and dust would be unusually high in areas with low solar radiation.
1.7.3 Increased Levels of Developmental Toxins within Many Childbearing Women: See Section 1.9.9 for details.
1.8 "Prevailing winds": This term should be defined here, since it will be used at various places later in this paper, and since it is subject to misinterpretation. It is the direction in which winds in a particular area tend to blow more often than in any other direction, and it is typically measured during a span of daytime hours, such as 7 AM to 7 PM, when wind speeds are normally higher than at night. But winds might be blowing in the prevailing direction less than 30% of the time overall and still be considered to be "prevailing." If emissions are produced in the evening or at night, they are likely to fall closer to the source and travel in a direction that's different from that of the usual daytime winds. The prevailing winds in most of the U.S., beginning somewhere north of the 30th parallel of latitude, blow toward the northeast; the 30th parallel crosses the southern U.S. approximately at the Gulf Coast of Mississippi. The "prevailing winds" on the West Coast are onshore, but that applies mainly during daytime hours, and there are many exceptions to that direction even during the day.
1.9 While Mental Disability has been Falling among Female Children and Rising among Male Children: Trends in Environmental Factors Associated with Autism and Retardation
As mentioned earlier, mental disability among girls dropped substantially in recent decades compared with females of earlier generations. <<Production of PCBs peaked in the early 1970s and was banned in the United States after 1979.
<<<Other neurotoxicants whose prevalence has declined: Dioxins that are far higher in leaded gas than unleaded. Dioxins from certain sources. Lead (refer to earlier sec and diags). "Releases (of dioxins) from industrial sources have decreased approximately 80% since the 1980s (U.S. EPA, 2004)".(National Report on Human Exposure to Environmental Chemicals Dioxin-Like Chemicals: Polychlorinated Dibenzo-p-dioxins, Polychlorinated Dibenzofurans, and Coplanar and Mono-ortho-substituted Polychlorinated Biphenyls Page updated April 2010 Centers for Disease Control and Prevention, Atlanta, GA 30333, accessed at http://www.cdc.gov/exposurereport/data_tables/DioxinLikeChemicals_ChemicalInformation.html)
<<<show data from other Aylward/Hays article 2002, showing steep decline in body burdens of dioxins>>
<<incorporate re rising popn and heating combustion, cf winter increase in MN dioxins>>
Some researchers have suggested that, because this phenomenon <increase in dioxins in env> has been observed worldwide, perhaps a
common source was responsible, with a proposed leading candidate being the combustion of and subsequent phase-out of leaded gasoline (Czuczwa et al., 1985a).
Quantitative estimates from these studies suggest that
rates of PCDD/F deposition increased more than 10-fold
from the 1930s to a peak during the late 1960s,(<mentned in Bfd secn>> and declined
by at least half from the peak by the late 1990s. (Regulatory Toxicology and Pharmacology, 37 (2003) 202 217 Dioxin risks in perspective: past, present, and future Hays and Aylward at http://acdrupal.evergreen.edu/envirohealth/system/files/Dioxin+risks+in+perspective.pdf )
The decline in dioxins in the environment was mainly in emissions from smokestack sources, which normally drift far enough to be deposited on agricultural lands where they become part of the food supply. So most of the food supply has probably improved. But dioxins contained in diesel emissions have increased greatly in the environment (see next section), and those emissions have probably settled substantially into bath tubs and outdoor pools in urban and suburban areas, in which the very vulnerable scrota (neurodevelopmental endocrine sources) of boys spend time soaking.
"there is a steadily expanding universe of chemicals and combinations of chemicals to which humans are exposed. Most of these chemicals have never been tested for developmental toxicity." (Scientific Frontiers in Developmental Toxicology and Risk Assessment (2000) Commission on Life Sciences (CLS) of National Academy of Sciences, p. 25)
1.9.1 Trends in diesel emissions, to which many people are substantially exposed: There have been substantial increases in recent decades in emissions from diesel trucks and many off-road diesel vehicles, including ships. The EPA provides data showing that, between the years 1987 and 2000 (2000 appears to be the latest year for which the EPA provides this data), dioxins released in diesel emissions increased about 100%: a 74% increase from off-road diesel emissions (including emissions from trains, ships, construction equipment and tractors) and a 134% increase from heavy-duty diesel truck emissions during that relatively short period.* ("An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000", EPA/600/P-03/002F, November 2006: especially Table 1-17. 2000 appears to be the most recent year for which the EPA provides national dioxin release data). With dioxins from diesel emissions increasing so dramatically, it is probably safe to assume that diesel emissions in general have also increased greatly. This is especially likely because diesel motors often continue in use for over thirty years in the U.S.; continued use of an ever-growing number of those motors, with their declining combustion efficiency, can be expected to have a cumulative effect on increasing diesel pollution levels. Except for newly-manufactured vehicles, emissions of diesel trucks and non-road diesel-powered vehicles/equipment are not regulated in most states in the U.S. <<refine this?>> (This is in contrast with the regular inspections typically required in Europe.)

Diesel emissions from offshore ships, having risen from smokestacks, will often be on a downward path by the time they reach some heavily-populated coastal areas. Statistics on changes in marine diesel emission exposures in the U.S. during the last decades are not readily available, but, with the major increase in international trade that took place during that period, they must have increased substantially. And, as explained in Section 1.4, those emissions are unusually toxic.
Fig. 2c (Source: r)
1.9.2 Indoor pollution increasing: There has been a reported decline (as of 2000) in emissions of dioxins and PAHs from a source that is very close to many infants and pregnant women: residential wood burning. But actual levels of toxins in indoor air may have been increasing even while amounts emitted were falling, because of residences' becoming more tightly sealed in recent decades. And there are several other sources of toxic indoor pollutants aside from wood burning, especially formaldehyde in plywood/pressedwood panels and DEHP in vinyl flooring.
1.9.3 DEHP (see Section 1.6.b) increasing: To people who have been observing the typical consumers' world in recent decades, it is probably apparent that use of flexible plastics as containers of food and beverages (including milk) has been increasing; and most of those plastic containers (including plastic film wrappers) contain DEHP. One relatively recent source of possible transfer of DEHP to foods that should be of special concern is the use of soft plastic film that covers frozen foods even while they are being cooked.
1.9.4 Increasing Use of Disposable Diapers (placing Dioxins extremely close to Glands that Produce the Neurologically Crucial Testosterone) : Usage of disposable diapers more than quintupled (to 1.93 million tons) in the U.S. between 1970 and 1980, and rose by more than an additional 40% by the year 2000.(article, "A Brief History of the Disposable Diaper", found at http://motherjones.com/environment/2008/04/brief-history-disposable-diaper)
1.9.5 <<moved>>
1.9.6 Releases from reservoir sources continuing: In addition to increases of emissions of certain toxins to the air, and increases in indoor toxins as indicated above, also substantial are continuing re-releases of old toxins stored in what the EPA calls "reservoir" sources. Dioxins are persistent in the environment, meaning that if they are sheltered from the degrading influence of sunlight, they can continue to be released to the environment in toxic form; such shelter could be found below the surface of the soil, in sediment at bottoms of lakes, inside vegetation, or inside chemically treated utility poles, railroad ties and wooden docks. The EPA points out that "…at least one-third of the overall risk to the general population from dioxin-like compounds comes from reservoir sources." (EPA/600/P-03/002F November 2006, p. 11-28) Dioxins are released into the air from soil through "volatilization," or in road dust, or when soil erodes, or in urban run-off, or in smoke from wildfires, or are leached out of chemically-treated wood (EPA/600/P-03/002F November 2006, p. 1-13). The re-released toxins land on surfaces with which infants come into contact, settle into lakes and streams, are absorbed into vegetation, and work their way up the food chain into animals and fish consumed by humans. The EPA considers forest fires and accidental fires at landfills to be the largest sources of such re-releases (EPA/600/P-03/002F November 2006, p. 1-37) As mentioned earlier, the EPA quotes studies estimating half-lives of dioxins in and below the surface of soil to be 9 to 100 years. "Runoff (of dioxins) from agricultural areas to surface waters is more than 100 times greater" than releases to waterways from known industrial point sources, according to the EPA. (EPA/600/P-03/002F November 2006, Section 11.3.1) The EPA says that dioxins do not dissolve well in water and that drinking dioxin-containing water is not a major source of dioxin body burden, but the EPA does nevertheless see fit to set a limit on the dioxin level permitted in water. Considering that dioxin levels are expensive to test for, one might wonder how many local water companies actually do such testing; and it is probably safe to assume that few homeowners with private wells have their water checked for dioxins. That would also apply to the sources of water provided to farm animals, whose meat and dairy-product fats end up in the human food supply. Given the various ways that dioxins in water can end up being ingested by humans, one might be less impressed to know that industrial releases of dioxins have declined substantially, knowing that the runoff of dioxins from agricultural areas to surface waters is 100 times greater than releases to waterways from industrial sources. Knowing about that toxic runoff from agricultural areas should also raise concern about time that developing boys spend swimming in lakes and streams flowed into by all of those dioxins (which are able to soak into the skin of the scrotum, probably reaching the sources of the testosterone needed for mental development).
To summarize some key points: While male mental disability has been increasing substantially, we have been seeing major increases in exposure of male infants to certain neurological toxins that are specifically connected with male brain development. Other major sources of toxins are at least stable. The implicated toxins that have been increasing, and their connections with male neurological development, are summarized here as follows:
a) major increases in DEHP, which can cause testicular atrophy, and which can therefore disrupt the supply of male hormones needed for normal brain development;
b) major increases in diesel emissions, which have been shown to suppress testicular function in male rats;
c) dioxins in soil accumulating unexpectedly rapidly. <<move some of this elsewhere?>> Because of their extremely long lives in soil, dioxins are continuing to rise even while the new amount added each year is declining; therefore soil often ingested by infants, and drinking and bathing water (especially if well water) and foods based on water coming from that soil, have been continuing to increase in dioxin content in recent decades. As will be described in Section 2.4, actual observed accumulations of dioxins in soil have turned out to be roughly ten times higher than the EPA had predicted in four cases, with no mention of predictions that had been any more accurate than that. The EPA acknowledges that they may have underestimated the effect of increases that result from long-term accumulation of toxins that degrade extremely slowly. Note that dioxins have been found to specifically harm the male glands that produce the testosterone that is essential for brain development. Also, it seems to be generally acknowledged in this author's polling among parents of both boys and girls that boys are more likely than girls to get dirty with soil; bear in mind that dioxins can be absorbed through the skin, and that thumb sucking sometimes continues into the period during which children (mainly boys) could be playing in soil;
(d) greatly increased exposure to dioxins in disposable diapers (see section 1.9.4), which rub against skin within 2-3 millimeters of the testicles;
(e) increasing PBDEs (and probably dioxins) in breast milk (see Section 1.2.d about the increase in breast feeding);
(f) bromine, in greatly increasing use as a substitute for chlorine in swimming pools, is known to be a neurological toxicant, and by its ability to penetrate the skin of partly-submerged infants it probably affects male production of testosterone needed for neurological development;
(g) almost certain major increases in other neurological toxins contained in the rapidly increasing diesel emissions (other than dioxins), including ones that very likely affect males more than females (see Section 1.9.1);
(h) extensive use of certain
pesticides, many new types of which were introduced in the 1980's; at least one
kind, chlorpyrifos, has been found to cause developmental deficits in male rats
without causing the same deficits in developing females (Chlorpyrifos
exposure during a critical neonatal period elicits gender-selective deficits in
the development of coordination skills and locomotor activity. Dam K at al.
Brain Res Dev Brain Res. 2000 Jun 30;121(2):179-87. PubMed - NCBI accessed at
http://www.ncbi.nlm.nih.gov/pubmed) Chlorpyrifos is the first pesticide
mentioned in a statement about insecticides that "have long predominated
for insect control on lawns, shade trees and shrubs, and nurseries." (Classes
of Pesticides Used in Landscape/Nursery Pest Management, Whitney Cranshaw,
Colorado State Univ., accessed Jan. 2012 at
http://www.entomology.umn.edu/cues/Web/042ClassesOfPesticides.pdf)
i) dimethylbenzathracene (Fig. 13a2) !!
1.9.7 Other Increasing Environmental Toxins that Might Also affect Males Predominantly: It is very possible that other neurological toxins that have been increasing in the environment in recent decades, in addition to the ones itemized just above, are also specifically toxic to males, but merely haven't yet been identified as such. (Bear in mind the importance of testosterone to development of the infant brain, as explained in Section 1.2.b.1) In the various studies of rats and mice exposed to toxins, which shed considerable light on effects of those toxins on humans, many effects of toxins are relatively easy to observe: lever-pressing behavior, hyperactivity, cleft palate, etc. Reduced testicle size, especially if significant but not major, might well go unobserved. More importantly, as found in the experiment by Watanabe et al. described in Section 1.4, reduction of testosterone output can be significant even though physical examination of the testicles does not reveal any effects. Detection of the inconspicuous effect requires major test procedures (described in that study) that are probably very rarely performed in tests of chemicals in the environment.
1.9.8 PAHs, which are basically products of imperfect combustion, have probably also been increasing not only with population growth but especially with the accumulating use of aging diesel engines whose combustion is becoming less efficient through the years. This author is aware of one PAH that is clearly an endocrine disruptor (see Figure 13a2), and apparently most of the others could be endocrine disruptors but have yet to be screened for that characteristic; and other PAHs are clearly implicated in harm to neurological development in general. ( Perera FP, et al. 2009. Prenatal airborne polycyclic aromatic hydrocarbon exposure and child IQ at age 5 years. Pediatrics 124(2):e195-202. Also Perera FP, et al. 2011. Polycyclic aromatic hydrocarbons-aromatic DNA adducts in cord blood and behavior scores in New York City children. Environ Health Perspect 119(8):1176-1181. )
1.9.9 Mercury is not identified as contributing specifically to male mental impairment, but it has been increasing in the environment and in the food supply during the period in question. According to the EPA, mercury in the atmosphere tripled between the era before human activity and current times.(EPA-452/R-97-006, December 1997, Table 2-3) A web page of the U.S. Geological Survey points out that, even though awareness of toxicity of mercury started in the 1950's, it wasn't until the late 1980's that investigations found high levels of mercury in fish commonly in northern-tier states and Nordic countries, and in the 1990's surveys found it in fish in other regions of the U.S. as well.("Mercury Contamination of Aquatic Ecosystems" at http://water.usgs.gov/wid/FS_216-95/FS_216-95.html ). (Mercury can drift thousands of miles in the atmosphere before settling on surfaces, and winds that prevail in most of the latitudes of the lower 48 U.S. states blow generally toward the northeast; so large amounts of mercury emitted from stacks would settle in northern areas first.) So there appears to have been an upward trend in in mercury in fish, which is major source of mercury ingestion by infants and child-bearing women, a trend that has been especially noticed during this last generation. And that recent increase is especially of concern because mercury found in greatest quantities in fish is the specific form (methylmercury) that is especially likely to affect humans; and "Recent research suggests that prenatal effects (on the nervous system) occur at intake levels 5-10 times lower than that of adults."(same USGS web page) The USGS quotes the best estimates as indicating that mercury in the atmosphere is increasing by about 1.5 percent per year. After finding a 15% increase in mercury in Minnesota lakes between 1996 and 2006, the first cause hypothesized by scientists was "mercury-spiked emissions from power plants around the world….atmospherically transported." (EPA newsletter, March, 2009)
In addition to the probable increase in average mercury per ounce of fish consumed during this period, total ounces of fish consumed by Americans increased 24 percent from 1980 through 1989.(National Marine Fisheries Service (2005), Silver Spring, MD (NOAA). Fisheries of the United States, 2004. Per Capita Consumption. Page 79,) Bear in mind that the 1980's appear likely to have been the approximate transitional period between gender-equal mental disability of earlier generations and the nearly two-to-one ratio of the last decades.
Although mercury is the best known contaminant that has been building up in fish, dioxins in fish are also a serious concern (see above), as is PCP (pentachlorophenol) that leaches out of preservative-treated wooden docks and then bio-accumulates in the fish. The latter two toxins, also, long persist in the underwater areas that are sheltered from solar radiation, and they are almost certainly increasing as more toxins flow into the water and as more PCP leaches out of docks every year.
1.9.10 Effectively a decline in beneficial sun exposure, following health advice of recent decades: Lower sun exposure leads to lower vitamin D levels. Vitamin D deficiency is associated with reduced immune function, and low immune function has been associated with autism in an NIH-funded study of autism.(d82) Also, according to an article in a publication of the American Medical Association, "Vitamin D deficiency can lead to reduced levels in the developing brain of calcitriol, a critical neurosteroid involved in brain development. Of interest, while health care providers have exhorted patients during the last 20 years to reduce sunshine exposure, autism prevalence has been increasing. It is also of interest to note that evidence indicates a substantial incidence of vitamin D deficiency in the United States and elsewhere among infants and toddlers."(d60)
1.9.11 Increasing Levels of Developmental Toxins to which Infants are Heavily Exposed, Prenatally and in Breast Milk:
In 1970 the average age of a first-time mother was about 21, and by 2008 the average age was 25.1(found at http://www.babycenter.com/0_surprising-facts-about-birth-in-the-united-states_1372273.bc , which drew statistics from the CDC and the Census Bureau); according to the Census Bureau's report for 2006, the peak age of fertility among women who had at least a bachelor’s degree was 30 to 34 years old, and a large number of births continued out to age 40 in that group. That is a large and growing sector of the population who are giving birth at an age by which they would have built up a far higher body burden of dioxins and mercury (and probably other toxins) than was typical in earlier generations. The burden would be higher both because of more years of accumulation and because of higher levels of toxins in their environment.<<insert specifics and source>> Women who had reached the age range of 40 to 44 in 2006 had an average of 1.9 children, compared with the average for women in the same age group in 1976 (3.1children). ( at http://www.census.gov/population/www/socdemo/fertility.html) The significance of that is that later children being breastfed receive lower levels of dioxins than earlier children being breastfed (average 20-30% decline just in going from the first to the second child, according to a study of samples from 153 breastfeeding women) ( Infant Exposure to Chemicals in Breast Milk in the United States: What We Need to Learn From a Breast Milk Monitoring Program, Judy S. LaKind et al., Environ Health Perspect 109:75–88 (2001) [Online 20 December 2000] at http://ehpnet1.niehs.nih.gov/docs/2001/109p75-88lakind/abstract.html ) So in the 2000's we have a sizable and growing number of infants with higher than the average historic exposure to levels of toxins (at least prenatally and probably also via breast milk), due to (a) the average mother's greater age, (b) increased levels of toxins in the environment, and (c) far higher proportion of children who are a first or at most a second breastfed child (breast-fed infants have levels of dioxins many times higher than those fed with formula -- see Section 1.2.d)
Figure 2e
This chart shows a record of the only data this author has been able to find about trends in dioxins in breast milk in the U.S. Organizations that promote unhesitating, as-exclusively-as-possible breastfeeding often quote a World Health Organization study finding that toxin levels in breast milk have been declining "in most industrialized countries;" but the U.S. is conspicuously absent in the data provided by WHO, including in all documents found in a detailed search of WHO's website in January of 2012. The European countries, data for which the organization does provide, have been more aggressive than the U.S. in combating pollution, from diesel combustion sources especially. (Dioxins in diesel emissions have been rapidly rising in the U.S. – see Section 1.9.1). Authors looking at data for the U.S. sometimes say that the trend in dioxins in breast milk here is "ambiguous" and that more data is needed. Unless they can show data other than what is shown in this chart, "ambiguous" seems to be a word that avoids recognizing an upward trend in the U.S. (Note that observations for the U.S. are shown with the darker dots on this chart.)
Part 2: More on Sources of Pollutants associated with Developmental Disabilities
As mentioned earlier, the EPA points out that dioxins are unintentional byproducts of several industrial chemical processes and of most forms of combustion, including forest fires, fuel emissions and waste combustion, and are included in the food we eat. Dioxins are "ubiquitous in the environment -- air, water, and soil", according to the EPA (34, Section 2.2). In the atmosphere the dioxins become attached to particulate matter and are typically deposited onto vegetation or other surfaces, especially via precipitation. Once on and in the vegetation, the dioxins affect humans when (a) consumed in affected food, especially animal-based foods from fish and animals that consume the affected vegetation, resulting in bio-accumulation, or (b) when re-suspended during residential burning and wildfires. Dioxins in the air are also deposited onto the ground and other surfaces (including indoors) with which infants come in contact.
<< show map of CA with these 3 standing out, away from urban areas/ combine with pesticide effect>> PAHs are apparently especially likely to be a product of imperfect combustion. This may help explain why three counties in California with very high rates of autism (Placer, Tuolumne and Mariposa) are counties in which there is considerable vehicular traffic at high altitudes, at which levels the vehicles' engines are normally not tuned for proper combustion. All (?) (most?) other California counties with high rates of autism are urban, where there is considerable vehicular traffic and/or industrial sources of dioxins and PAHs.
Since most people are surprised to be told that burning of wood and eating freshwater fish can be sources of neurological toxins, additional attention to that subject will be given below. It will be assumed here that there is no need to dwell on the sources indicated in bold above or on other sources mentioned earlier, but that should in no way imply that those are not similarly substantial sources.
2.1 Burning of Wood and Foliage Emits Toxins
Combustion of wood is known to emit dioxins and lead (26) as well as PM and methanol. According to tests by Nestrick and Lamparski, burning 1 kilogram (2.2 pounds) of wood produced as much as 160 micrograms of total dioxins. (Keep in mind that, as explained above, dioxins and other endocrine disruptors adversely affect neurological development, and that there is good evidence that they "can affect test animals’ bodily functions at very low levels — well below the “no effect” levels determined by traditional testing.") The same research found that lead produced from burning one kilogram of wood was 0.1mg to 3 mg. Keep in mind the EPA's finding that any amount of lead can be harmful, especially to children. Another source, calculating on the basis of EPA data, estimates that dioxin emissions from forest fires exceed all other U.S. sources of dioxin emissions combined.(27)
The EPA lists residential wood combustion as the largest source of PM 2.5 in California, producing almost 40 tons of those emissions in that state in 2005 alone (well above the totals for both industrial processes and on-road vehicles), and "fires" (mainly forest fires/wildfires) are listed as the fourth-highest source.(28) Adding tremendously to the significance of the above is that so much of this pollution originates inside residences, where part of it escapes directly into the indoor air breathed by infants and pregnant women. The remainder is emitted into the nearby community's air, from where it becomes part of the general air supply breathed by infants and pregnant women in that area. It should be of special concern that this largest-in-all-of-California source of PM 2.5 tends to be concentrated in certain Northern California areas and communities, where the climate is colder and the wood supply is especially plentiful. Burning of brush (in backyard burning and wildfires) is not specifically known as a source of lead, but it is a known source of dioxins (28a) and it almost certainly emits particulate matter.
<<expand>>Toxicity especially strong if preservative-treated wood or trash is included.
Foliage and wood (as well as fossil fuels) contain the three elements which, when chlorine is present during combustion, can produce dioxins. The final ingredient (chlorine) can be provided by atmospheric pollutants or by the plastics in typical trash. This potential for creating dioxins during burning of organic matter is present even when the fuel doesn't already contain toxins. But in addition, vegetation also typically absorbs and retains existing toxins (which can be re-suspended during burning). It appears to be generally agreed, including in research by NASA, that many houseplants are effective at reducing indoor pollution because they absorb toxins from the air (through openings normally on the undersides of the leaves). Outdoor vegetation can be expected to do that same absorption of toxins. The toxins will probably remain contained within the plant or tree, continuing to accumulate through the years for longer-lived vegetation. Those stored toxins will almost certainly be dispersed into the air when the vegetation is burned during wildfires. (Obviously, the effect would be reduced if some toxins had travelled to the roots.) So residential burning as well as wildfires could be expected to be substantial sources of toxins able to be re-suspended into the air, especially if much of the vegetation burned is years old. This re-suspension is in addition to the creation of dioxins that takes place as a result of the burning. Residential burning is especially likely to create toxins if it isn't done correctly, and it probably isn't done correctly a very high percentage of the time.
2.2 An Apparent Incongruity between the Recent Increases in Autism and the Long-Standing Existence of Wood Burning:
Q: Why, if we claim a causal connection as stated above, should autism have been increasing substantially in recent decades? After all, burning of wood is not at all a recent development.
A: First, wood burning is only one of several important sources of neurological toxins. More importantly, wood and vegetation emit harmful levels of dioxins when burning because of
(1) chlorine, essential for creation of dioxins, being provided by increasing sources in the environment; those sources include atmospheric hydrochloric acid and other increasingly common waste stream sources of chlorine (including PVC, or polyvinyl chloride plastic) that could be included with the burning;
(2) increasing pollution from human sources that has caused wood and vegetation to be receiving and absorbing toxins at increased rates, creating the potential for re-suspension of existing toxins during combustion
2.3 Toxins in Freshwater Fish:
Fish consumption makes up about one-third of the total general population's CDD/CDF TEQ (dioxin) exposure.* *(EPA/600/P-03/002F November 2006, P, 11-28) Toxins including mercury, dioxins and PAHs are deposited into lakes via atmospheric deposition, via streams, or via runoff from pavement and land following rain or snow. Those lakes are in basins that also collect wood-burning emissions, which affect infants living near the shores of the lakes. (After originating from human-generated pollution, those toxins enter bodies of water and pass up the food chain from sediment to game fish, whose flesh is tender and seemingly well suited to feeding infants.) A "National Dioxin Study" found that fish from the Great Lakes region were among the most severely contaminated in the United States. (7b, Section 5.4.4). Probably even worse are fish in densely-populated, industrial Rhode Island, where the state government tells people not to eat freshwater fish caught anywhere in the state, with the exception of trout that are added from outside the state's normal waters. There is nothing inherently toxic about fish and lake water; those would normally be fine in North Dakota or much of Canada. The toxicity comes mainly from precipitation and drainage into the lakes from environmental pollution, combined with (as mentioned earlier) leaching of PCP from preservative-treated wooden docks.
2.4 A Major Source of Ingestion of Neurological Toxins for Young Infants: Eating Non-Food Substances
According to the Seattle/King County, WA Public Health website, " infants and toddlers often eat dirt and other non-food items,…. Some little children just put everything into their mouths as a mode of exploration." The NIH's Medline Plus encyclopedia refers to "pica", the condition of deliberate eating of non-food substances on a consistent basis, as affecting 10% to 32% of children ages 1 to 6. Since this eating of non-food substances applies to a significant proportion of infants even when those who do it inconsistently are not even included in that percentage, that implies that this means of ingesting possibly toxic substances in harmful quantities could be very common. The Seattle Public Health website quoted above, and authors for Medscape.com quoted below, say that pica isn't even considered to be pathologic with reference to infants below age two, apparently in recognition of how extremely common it is for younger infants to put non-food items in their mouths and ingest them. Bear in mind that below age two is a period during which the infant brain is going through critical stages of development. And bear in mind the extremely long lives of dioxins in soil, which means that dioxins continue to accumulate to ever-higher concentrations in soil, as more and more is deposited through the years.
It is apparently difficult to grasp how high concentrations of dioxins in the soil can become as they accumulate through the years, even for the EPA's scientists. The EPA acknowledges that actual levels of dioxins observed in four reports on rural soil concentrations in the U.S. exceeded their predictions by amounts in the range of 1000%. Nothing was mentioned about any estimates that had turned out to be any more accurate than that. The EPA acknowledged that they may have greatly underestimated the effects of accumulation of dioxins through the years, overestimating the extent of degradation that would take place.(at http://www.cqs.com/epa/exposure/part2_v1.htm "Estimating Exposure to Dioxin-Like Compounds," EPA, revised 1992; III.6.2)
<<replace with below?>According to two MD's writing for Medscape.com (at. http://emedicine.medscape.com/article/914765-overview), pica "is the most common eating disorder in individuals with developmental disabilities." Considering the known developmental toxicity of dioxins that can be extremely high in soil, it would not be surprising if a cause-and-effect relationship (starting with pica) were at the basis of this typical association.
Medscape article: "Pica is an eating disorder typically defined as the persistent ingestion of nonnutritive substances for a period of at least 1 month at an age at which this behavior is developmentally inappropriate (eg, >18-24 mo). The definition is occasionally broadened to include the mouthing of nonnutritive substances. Individuals who present with pica have been reported to mouth and/or ingest a wide variety of nonfood substances, including, but not limited to, clay, dirt, sand, stones, pebbles, hair, feces, lead, laundry starch, vinyl gloves, plastic, pencil erasers, ice, fingernails, paper, paint chips, coal, chalk, wood, plaster, light bulbs, needles, string, cigarette butts, wire, and burnt matches.
In children aged 18 months to 2 years, the ingestion and mouthing of nonnutritive substances is common and is not considered to be pathologic."
Among the mentally
retarded, the relatively common occurrence of pica
is reported to be positively correlated with degree
of retardation (Broadening the Perspective of
Pica: Literature Review
ELLA P. LACEY, PhD at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1579989/pdf/pubhealthrep00198-0031.pdf)
Distances over which Neurological Toxins in the Air Affect Human Infants and Pregnant Women:
The study of effects of proximity to California freeways (referred to in Section 1.4) found a considerably elevated percentage of cases of autism among infants residing within about 1000 feet of a freeway. 24b) Beyond that (for the approximately-three-mile width of the area studied), there seemed to be little change in autism levels depending on distance from the freeway. But the study was conducted in what is considered by the Census Bureau to be urban areas, where general pollution levels are normally high compared to non-urban areas. As this paper will attempt to demonstrate, greater distances from busy highways (beyond the 1000-foot threshold) may have beneficial effects if the region studied extends into non-urban areas that don't have their own serious pollution sources.
Figure 2a5
The big question is the distance that non-road combustion emissions will travel and still seriously affect people. As opposed to vehicular emissions that originate very close to ground level and therefore affect people nearby, emissions from tall smokestacks from power plants, large factories, and large ships are initially emitted high above the surface and are directed upward; then the heat of the emissions keeps carrying them still farther upward for some time after exiting the stacks. The wind carries them for many miles, until eventually major parts of the emissions are deposited onto surfaces. Some are likely to be deposited relatively nearby, possibly starting a few miles downwind from the source. At the other extreme, one of the most neurologically toxic emissions, mercury, can travel around the world before being deposited. Pennsylvania, New York, and the New England states requested that the EPA require reductions in emissions from facilities as much as 550 miles and more upwind from them, on the basis of atmospheric pollution in the northeastern states caused by emissions from 22 states to their south and west, and the EPA agreed (see Section 4.4.2). Precipitation considerably promotes deposition of pollutants.
Data from the EPA can help one determine where pollutants are highest, but those data should ordinarily be considered as only educated approximations when looked at below the state level, since monitoring stations are often placed in only about one out of four counties, if there are monitoring stations at all for the particular pollutant under consideration.
Part 3: Effects of Climate, and Probably of Vitamin D, on Sources of Disabilities
3.1 In areas with more sunshine, dioxins are much less likely to be created and/or to continue in toxic form, as will be explained:
3.1(a) Creation of dioxins requires chlorine, the active form of which is reduced by sunshine: Dioxins are created during combustion of organic materials; but the element chlorine must be present, since chlorine is an essential part of every molecule of dioxin. Low concentrations of chlorine are normally present in the atmosphere in any area where pollution is present, incorporated into hydrogen chloride (HCl). HCl becomes dissolved in water vapor in the form of hydrochloric acid and is one of the three "most abundant sources of chlorine available for participation in the formation of CDDs/CDFs (dioxins)…" (d57b) But sunlight can dry out the water in which the hydrochloric acid is dissolved, leaving the HCl relatively unreactive and unlikely to support formation of dioxins during combustion. <<cite ref>>
3.1(b) Creation of dioxins is promoted by colder temperatures: Dioxins have been found to be typically formed at cooler temperature ranges of combustion.<<cite ref>> Combustion in cold areas is likely to take longer to reach hotter operating temperatures, and the combustion chamber is more likely to descend into the cooler part of the operating range during idling of motors, during intermittent operation of incinerators, or when heating levels are turned down. Furnaces and wood-burning stoves in very cold states would almost certainly be larger than average. That should be considered in light of standard anti-pollution advice to use wood stoves that are the smallest that can provide the needed heat, since turning a fire down low is known to produce more toxins than a hot fire. Stoves that are big enough to keep a house warm during an entire Maine or Minnesota winter would certainly tend to be kept at a low flame during the fall and spring.
Background levels of dioxins in air were measured in a Minnesota location about 25 miles northwest of Minneapolis-St. Paul, with no major industrial or commercial activity occurring in the area. Ambient air samples were collected in the winter and summer of 1988, checking for levels of two different varieties of dioxins. The differences between summer and winter levels were quite remarkable, with maximum average levels of one variety being 17 times higher in the winter than during the summer, and maximum average levels of another dioxin variety being 342 times higher during winter than during the summer.(p. 427 of ATSDR 1998 publication) The author of the study attributed the differences to increased emissions from combustion sources during the winter, and that certainly seems to be a logical assumption, especially considering that Minnesota is a very cold state during the winter. Such wintertime readings were not readily available for other states, but it is probable that wintertime increases in neurological toxins are unusually high in Minnesota, with its unique combination of very cold temperatures and substantial city population. (Minnesota has 17 of the 21 coldest U.S. cities with populations over 50,000, per city-data.com.)
3.1(c) Potency of dioxins (and PAHs) declines with greater exposure to sunlight: Dioxins are subject to destruction by sunlight, within a few days (34a and 7b). Intensity of sun exposure has been seen to be the main variable affecting the lifetime of the dioxins in atmosphere. So it is very likely that dioxins emitted into the atmosphere in high-solar areas would be completely degraded before they ever land on the vegetation that will subsequently enter the food chain or be burned; if not before, then soon after deposition. In regions with lower amounts of sunlight, or even in heavily-shaded local areas within high-solar regions, dioxins would be far more likely to retain their toxicity; and they would probably then keep accumulating into increasingly potent concentrations in the vegetation or soil, unless they are degraded by solar radiation that reaches surfaces of those substances. If dioxins in the vegetation don't enter the food chain directly or degrade, they normally eventually become part of the soil, from where they could be recycled on the way to human ingestion. Or the dioxins might also be re-suspended in a wildfire and thereby form atmospheric concentrations affecting downwind infants and mothers-to-be. If dioxins accumulating in forest soil aren't re-suspended in fires, they can be transported by soil erosion (aided by unpaved roads) that goes to bodies of water, ending up in fish eaten by women and infants.
The above probably helps to explain why two of the three states with the highest rates of autism in the U.S. (Minnesota and Maine) are at the far northern border of the contiguous states, and the other one of the top three (Oregon) is near the northern border. In addition to extending the toxic lives of dioxins, low sunlight goes along with lower temperatures, and dioxins are known to be created especially in the lower ranges of combustion temperatures. In sunnier locations, high engine operating temperatures are likely to be reached sooner during wintertime, and ongoing combustion is more likely to be sufficient to keep the combustion chambers of engines, stoves and fireplaces steadily at high temperatures.
3.2 Other Things related to Reduced Vulnerability of Infants to the Effects of Toxins in Areas of Greater Sun Exposure:
(a) Greater sun exposure leads to higher vitamin D levels. Vitamin D deficiency is associated with reduced immune function, and low immune function has been associated with autism in an NIH-funded study of autism.(d82)
(b) Residential wood fires and wood-burning stoves are known sources of PM, dioxins and lead, and most children in areas with greater warming effects from sunshine would almost certainly have comparatively lower exposure to those sources. As noted in section 2.1, the EPA considers residential wood burning to be the largest source of PM 2.5 in California. As is the case with wildfires, quantity of dioxins emitted by the burning depends partly on exposure the firewood has had previously, including to sunlight.
(c) Children in areas with more sun and in areas with less rain are likely to spend less time indoors, where, according to the EPA, pollution "may be two to five times higher than outdoor levels." (10/20/10 EPA press release). Obviously being outdoors while there is a fire in the vicinity would be bad; and outdoor air in urban areas or near major highways appears generally also to be worse than indoor air (EPA/600/8-90/057F May 2002 Health Assessment Document for Diesel Engine Exhaust National Center for Environmental AssessmentOffice of Research and Development U.S. Environmental Protection Agency Washington, DC, p. 2-113); but during normal times in areas with average or lower pollution, being outdoors more and having the windows open wider would probably benefit the infant's general health and ability to tolerate sporadic environmental toxins.
The case of the Los Angeles area: A study published in 2010 found Los Angeles-area neighborhoods whose children had "approximately four times greater risk of autism than those born in any other place in California." (THE SPATIAL STRUCTURE OF AUTISM IN CALIFORNIA, 1993–2001 Mazumdar et al., http://www.ncbi.nlm.nih.gov/pmc Health Place. 2010 May; 16(3): 539–546. Published online 2010 January 22.) As indicated by the source cited in Section 1.2.d, population characteristics that are associated with high levels of breastfeeding are higher educational levels and white ethnicity. In the high-autism cluster area of Los Angeles, the median property values in the various neighborhoods ranged from $300,000 to $500,000, while values in the comparison zone ranged from $150,000 to $175,000. Also, 62% of the population in the high-autism area is white, compared with 41% in the comparison zone.
In addition: The EPA says that much more dioxin intake results from food consumed than from air breathed, and that generalization no doubt applies well to the average infant and average child-bearing woman. But the air supply in this high-autism area is very different from the average. Los Angeles is famous for its smog, which has a tendency to be trapped in a basin for extended periods. <<insert graphics from article, topog of area>> This topographical map shows a low area, almost surrounded by ridges and mountains, that seems very similar to the high-autism area found in the above study. Pollution, especially diesel pollution (see Section 1.4 for details on that), from offshore as well as from truck traffic, would be blown into this area by the normal on-shore daytime winds, and would typically then be impeded by the mountains on the eastern side of this basin. In most areas, the polluted air could drain out of the area at night, but in this area it would be largely trapped. <<insert graphics showing on-shore/offshore winds; likelihood of PM being deposited, like precip or with precip, on windward sides of mountains; forming high-dioxin dust and soil that infants ingest; maybe also Tuolum/Marip >> Bear in mind, as noted in Section << >>, that dioxin releases in both on-road and off-road diesel emissions have been increasing very rapidly as of the most recently-published EPA data.
High-meat/fat diet more likely in high-autism area, because of income differences and lower Hispanic pop, which would affect infants in utero and via breast milk:
<<Move 1000-ft /hi-aut study art to here?>>
Topographic map from http://www.sci.sdsu.edu/salton/SaltonTopographicL.jpg
Keywords: causes of autism, considerations regarding breastfeeding, disadvantages of breastfeeding, environmental toxins, neuro-developmental toxins
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(1) U.S. Census Bureau Table B18104: SEX BY AGE BY COGNITIVE DISABILITY Universe: Civilian non-institutionalized population 5 years and over. Data Set: 2008-2010 American Community Survey 3-Year Estimates (accessed Jan. 2012 at http://factfinder2.census.gov , using their search process) The ratios quoted were arrived at by looking at the percentage reported for each sex in the various age groups, providing data based on the following question: "Because of a physical, mental or emotional condition, does this person have serious difficulty concentrating, remembering, or making decisions?" The even ratio of mental disability among people born during the mid-to-late-mid 1900's, becoming very uneven later, is compatible with various studies, as per the following statement about mental disabilities in the U.S.: "Almost all studies report… especially among children less than 15 years of age… males have about a 1.5-fold greater prevalence….. Gender differences are not evident among adults." (Leonard et al. 2002; Gissler et al. 1999)." (emphasis added) This quotation taken from Maulik PK, Harbour CK, 2011: Epidemiology of Intellectual Disability. In: JH Stone, M Blouin, editors. International Encyclopedia of Rehabilitation. Available online: http://cirrie.buffalo.edu/encyclopedia/en/article/144/ ) Note that the quoted ratio of 1.5 to 1 appears to be applied to the general population, not to children specifically; it was merely stated that the difference between the disability levels of the two sexes is especially large among children. To arrive at a general ratio of 1.5 to 1 when there is no gender difference in prevalence among most adults, the ratio among children has to be substantially more uneven than 1.5 to 1.
(1a) This category increased greatly from about one in 1500 reported in the early1990's to about one in 100 in 2007, during the same major period of mental disability increase that we are concerned with. Since about 1% of all infants currently being born will eventually be diagnosed with autism, and since the male-to-female ratio for autism is about 4.3 to 1, the percentage of boys who are currently becoming autistic would be over 1.6%. Of that 1.6%, less than half are considered to be retarded. There are mental health professionals who say that the autism figures have risen solely because of changes in awareness of the disorder and substitution of diagnoses of ASD for diagnoses that in earlier years would have indicated other disabilities. They often point to the similarity between current totals of mental disability figures of various kinds and what the totals were 20 years or so ago. But those who say autism hasn't actually increased greatly don't seem to take into account the major shift that has taken place in the proportion of boys to girls among children with mental disabilities, which is best explained by rise of disabilities (such as autism) that affect the two sexes in greatly different proportions.
(1b) "The Epidemiology of Autism Spectrum Disorders*, Craig J. Newschaffer,1 et al., Department of Epidemiology and Biostatistics, Drexel University Drexel E-Repository and Archive (iDEA) http://idea.library.drexel.edu ANRV305-PU28-21 ARI 22 December 2006 7:53. Also a CDC web page at www.cdc.gov/ncbddd/autism/data.html
(2a) NIMH Director's blog at http://www.nimh.nih.gov/about/director/2009/nimhs-response-to-new-hrsa-autism-prevalence-estimate.shtml
(2) "On-Road Sampling of Diesel Engine Emissions of Polychlorinated Dibenzo-p-Dioxin and Polychlorinated Dibenzofuran," by Brian K. Gullett, Jeffrey V. Ryan, U.S. EPA, Air Pollution Prevention and Control Division (MD-65), National Risk Management Research Laboratory, Research Triangle Park, NC, article found at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=23969#Download
(3) EPA's Proposal to Designate an Emission Control Area for Nitrogen Oxides, Sulfur Oxides and Particulate Matter, Technical Support Document, Chapter 3: Impacts of Shipping Emissions on Air Quality, Health and the Environment At http://www.epa.gov/otaq/regs/nonroad/marine/ci/420r09007-chap3.pdf , with the passage regarding marine diesel emissions found in Section 3.3.1.3 )
(4) from NIEHS/NIH website at http://www.niehs.nih.gov/health/topics/agents/endocrine/index.cfm)
(5) from http://www.niehs.nih.gov/health/docs/endocrine-disruptors-2010.pdf)
(6) Committee on Developmental Toxicology, Board on Environmental Studies and Toxicology, in Scientific Frontiers in Developmental Toxicology and Risk Assessment (2000) , Commission on Life Sciences, The National Academies Press, p. 56
(7) United States Office of Research May 25, 2001 Update, Environmental Protection and Development Agency, Dioxin: Scientific Highlights from Draft Reassessment (2000)
(8) Judy L. Cameron, Dept. of Psychiatry, Neuroscience, and Cell Biology and Physiology, University of Pittsburgh, in "Effects of Sex Hormones on Brain Development," Chapter 5 of Handbook of Developmental Cognitive Neuroscience, MIT Press, 200, edited by Charles A. Nelson and Monica Luciana. Charles A. Nelson is Research Director, Developmental Medicine Center at Children's Hospital Boston, and Professor of Pediatrics and Richard David Scott Chair in Pediatric Developmental Medicine Research at Harvard Medical School; Monica Luciana is Associate Professor of Psychology and Child Development at the University of Minnesota.
(9) ”Steroid Hormones and Brain Development: Some Guidelines for Understanding Actions of Pseudohormones and Other Toxic Agents" by Bruce S. McEwen, Laboratory of Neuroendocrinology, Rockefeller University, New York, NY (published in Environmental Health Perspectives Vol. 74, pp. 177-184, 1987). Research in the author's laboratory was supported by NIH Grant NS07080 and NIMH Grant MH41256. Institutional support from the Rockefeller Foundation for research in reproductive biology was also acknowledged.
(10) Stephen B. Klein and B. Michael Thorne in their Biological Psychology (2006), Worth Publishers, p. 390
11b: Sex matters in autism and other developmental disabilities, Thompson, Caruso and Nellerbeck, Journal of Learning Disabilities , Sage Publications, London,Thousand Oaks and New Delhi p. 352, referring to COLLAER, M. L. & HINES, M. ‘Human Behavioral Sex Differences: A Role for Gonadal Hormones during Early Development?’, Psychological Bulletin
(14) Committee on Developmental Toxicology, listed above
(15) Sherry G. Selevan, Carole A. Kimmel and Pauline Mendola, National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency, Washington, DC, USA)
(16) in "Epidemiologic Evidence of Relationships Between Reproductive and Child Health Outcomes and Environmental Chemical Contaminants", published in Journal of Toxicology and Environmental Health Part B, Volume 11, Issue 5 & 6 May 2008 , pages 373 – 517
(17) Winter JS, Hughes IA, Reyes FI, Faiman C, "Pituitary-gonadal Relations in Infancy", Clin Endocrinal Metab 1976, 42:679), (as reported in Principles and Practice of Endocrinology and Metabolism, by Kenneth L. Becker 2001 (p. 914))
(19) found at http://water.epa.gov/learn/training/dwatraining/upload/dwaNPDWR-risktoruletraining.pdf p. 1-58
(20) "Particulate Matter (PM) Research Centers (1999–2005) and the Role of Interdisciplinary Center-Based Research", (Fanning et al.), p.4, found at http://www.epa.gov/ncer/science/pm/documents/11543.pdf
(23) Found a http://www.niehs.nih.gov/research/supported/centers/core/grantees/rochester/index.cfm "Previous studies indicate that UFP (ultrafine particles) can translocate ...... to extrapulmonary organs …. within 4 to 24 hours post exposure. Additional studies were designed to determine whether translocation of inhaled UFP takes place to regions of the brain, ...We demonstrated ..... increases in the striatum (a section of the brain), frontal cortex, and cerebellum. .....We conclude that the olfactory neuronal pathway is efficient for translocating inhaled UFPs to the central nervous system ....."
(24) in the EPA's Health Assessment Document for Diesel Engine Exhaust (2002), in the section that deals with bioavailability of organic constituents present on diesel exhaust particulates (specifically in sections 3.5.3 and 3.5.4)
24b "Residential Proximity to Freeways and Autism in the CHARGE Study" , Environmental Health Perspectives,
Published in 119(6) Jun 2011, Heather E. Volk 1, Irva Hertz-Picciotto 2, Lora Delwiche 2, Fred Lurmann 3, Rob
McConnell 4 1 Departments of Preventive Medicine and Pediatrics, Zilkha Neurogenetic Institute, Keck School of Medicine, Children’s Hospital Los Angeles, University of Southern California, Los Angeles, California, USA, 2 Department of Public Health Sciences, University of California–Davis, Davis, California, USA, 3 Sonoma Technology Inc., Petaluma, California, USA, 4 Department of Preventive
Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, USA