Environmental Factors that may be Leading to Shorter Lifespans in the U.S.
by DP Meulenberg
Contents and brief summary:
Section 1: Death rates have recently been increasing in the U.S., and there has been a distinctive pattern in those increases: They are apparent in a broad central age range (5-64) while continued declines in death rates are seen at either end of the lifespan. Identifying exposures that could have contributed to such an unusual pattern might enable society to learn how to reduce adverse effects, thereby saving many lives.
Section 2: Two highly-toxic chemicals: PCBs and dioxins; when and how they affect people:
Section 2.a: Rapid increases of PCBs and dioxins in the U.S. environment in the mid-20th century
Section 2.b: Increases in human intakes of PCBs and dioxins in the post-1950 years.
Section 2.c: Development as a life stage of special vulnerability to chemicals such as PCBs and dioxins.
Section 2.d: Many serious effects of PCBs and dioxins, especially in the long term.
Section 3: The basic pattern of death-rate increases in relation to the post-1950 increases in PCBs and dioxins:
Section 3.a: This pattern as seen in recent years: (a) increasing deaths in people who are in the age range, mostly born after 1950, who received greatly increased developmental exposures to PCBs and dioxins, but (b) with little or no increasing deaths in people in whom long-term effects of those toxins had too little time to develop (young children).
Section 3.b: Looking back farther in the data, we see a (less conspicuous) occurrence of the same pattern of increased death rates in relation to likely long-term effects of developmental exposures to PCBs and dioxins; death rates increased at times that are very compatible with earlier times of increased developmental exposures to PCBs and dioxins.
Section 4: Presence of PCBs and dioxins in the environment, as compared with exposures of developing children.
Section 4.a: Exposures of vulnerable, developing infants to the toxins may differ from and matter much more than presence of the toxins in the general environment.
Section 4.b: What it is that seems to determine higher versus lower exposures to PCBs and dioxins during the vulnerable developmental period.
Section 4.c: Exposures that far exceed established safe levels
Section 4.d: Historical changes that affected infant exposures to PCBs and dioxins in the U.S.
There are good reasons why exposures from an earlier decade, with effects that have long been latent, could be affecting death rates now.
Section 5: One age group has shown very unusually favorable outcomes, and we might learn something useful from that..
Section 5.a: The 45-54 age group has been an exception to the death rate increases in the central age range.
Section 5.b: This age group, with its notably favorable outcomes, was born basically in the 1960's, which were a low period for infant exposures to PCBs and dioxins; reductions in exposures to those toxins may have led to the favorable outcomes.
Section 5.c: Are the recent death rate increases the new normal? There are good reasons to see them as such, with implication of a pressing need for appropriate response.
Section 5.d: The opioid epidemic
Section 6: Other examples of PCB/dioxin exposures' being related to adverse health outcomes and death rates, with more favorable results among the less-exposed (45-54) age group:
Section 6.a: Cancer is understandably related, since PCBs and dioxins are carcinogens. The 45-54 age group had the most favorable death rate outcome of all age groups in this category in recent years.
Section 6.b: Porphyria is very possibly a death-related outcome of the normal combined exposures to PCBs and dioxins.
Section 6.c: Suicide (a) among teenagers is very likely linked to endocrine disrupting effects of PCBs and dioxins and (b) in rural areas is probably linked to dioxin emissions resulting from the rural practice of backyard burning that has included plastics since about 1950. The 45-54 age group had the most favorable death rate outcome of all age groups in this category also, in recent years.
Section 7: Additional reasons for concern about PCBs and dioxins: Among young people who (as a group) have received greater exposures to PCBs and dioxins in recent decades, there have been large increases in obesity, diabetes, allergies, behavioral and learning disorders, activity limitations, and intellectual impairment. Increases in cognitive impairments have been especially high among children in specific types of families whose children would have had the greatest developmental exposures to PCBs and dioxins.
Most of the population of U.S. young people has been failing to meet the basic health standards for military service in recent years.
Section 8: Other, more-recently high toxins (flame retardants) that would have added to effects of PCBs and dioxins
Conclusion: The distinctive age-group profile of the recent death rates could be largely explainable according to the recognized long-term effects of PCBs and dioxins. There have been many increases in death rates in specific age groups at certain times that are very compatible with long-term causation by PCBs and/or dioxins, to which vulnerable infants were exposed in increasing amounts at relevant times during development.
There have also been increases in physical and mental health impairments among children and young people in recent decades, which have apparently been higher among those groups that would have had the greatest exposures to PCBs and dioxins as infants.
Something effective can be done to reduce future exposures of developing infants to the adverse effects of these toxins, without causing verifiable risk in other respects.
There has recently been attention paid to the data indicating that the historically normal trend toward longer lives has been stopped and slightly reversed in the U.S. This development was observed for 2014-2015 and 2015-2016, and it has occurred for the third year in a row for 2016-2017. By now it ought to be considered to be something resulting from underlying causal factor(s) in the environment, which should be investigated and dealt with so as to minimize them.
First, it should be pointed out that the data being discussed here merits greater respect than that of much of the health-related research, since this data is "not subject to sampling error," in the words of the CDC;11 it is not based on polling of a (possibly unrepresentative) sample of the population, as is the case in typical studies, but instead is based on tabulation of the full count of death reports. Multi-year increases of death rates, departing from the historical, favorable trend, deserve to be taken seriously.
Section 1: The basic pattern of the increasing deaths: apparent only in those in the 5-64 age range
(Above table accessed at https://www.cdc.gov/nchs/data/hus/2017/021.pdf)
It is easier to understand the relations of the above individual statistics to the overall picture if they are viewed in graphic form, as shown below:
As seen here, all of the age groups that showed increasing death rates were in the 5-to-64 central age range. The only age group that does not conform with the rest of that age range is the 45-54 age group, which is a meaningful exception and will be discussed later.
That leaves two separate age ranges of people who have not been significantly affected by the recent adverse mortality trends: (a) young children, and (b) people age 65 and older (as of 2016).
Since publication of the document from which data for these charts was taken, updated data (for 2017) for most of the age groups has been published.12 With the most recent figures added in, the overall pattern seen in these charts (the same bars being black in the central range and green at the ends), would remain.
So there is compelling reason to look into any exposures to adverse influences in the environment that might have strongly affected the large central part of the population while having little or no effect on those at either end of the life span. Identifying any exposures that could have contributed to such a pattern might enable society to address the exposures and possibly prevent their continuation or at least reduce them, thereby saving many lives.
Section 2: Two highly-toxic chemicals, PCBs and dioxins, started to become substantially present in the U.S. environment beginning in the late 1940's (see Section 2.a below), although both declined later in the century. PCBs are ranked by the U.S. Agency for Toxic Substances and Disease Registry as being among the top 5 priority hazardous substances.27 Dioxin is "often called the most toxic man-made chemical" as stated in a document of the EPA, with no question expressed about the correctness of that assessment.28 Exposures to developmental toxins such as these during early childhood have been increasingly recognized to have major effects later in life. (more on this later)
In line with the timing of Americans’ exposures to PCBs and dioxins (which will be discussed below), PCBs and dioxins would have had developmental effects mainly only on the age groups born in the 1950's and later; notice that the black bars in Figure 2 above, representing age groups with increasing death rates, apply only to people born in 1950 and later.
PCBs and dioxins both have serious long-term effects, to be described in Section 2.d later, but background-level exposures to them are not reported to be life-threatening in the near term; this can explain why young children continue to show declining death rates on the above chart even though their exposures to PCBs and dioxins during infancy have very likely actually been at hazardous levels.
Section 2.a: PCBs and dioxins rapidly increased in the U.S. environment in the mid-20th century:
PCBs: Production of PCBs (not yet known to be toxic at that time) began in the 1920's but only reached substantial volume after 1945, according to a working group of the International Agency for Research in Cancer;13 they were used in various kinds of electrical equipment and in many areas of manual work.14 Presence of PCBs in the U.S. environment increased greatly in 1949 and later, when they came to be widely used in various types of building materials.15
Dioxins: Burning of plastics is known to emit dioxins to the air.16 EPA, NIH, and MIT publications substantiate that plastics contained in trash produce dioxins when trash is burned (see Appendix A), helping to create the major dioxin emissions that the EPA knows to result from household and farm burning of trash.17 Backyard burning of trash that contains plastics would have become widespread (especially in rural areas, but also in municipal and hospital incinerators) within a few years after large-scale production of plastics began in the late 1940's; plastics production in the U.S. (especially for consumer goods) expanded dramatically after the end of World War II (1945).18 Also, evidence provided by the U.S. Agency for Toxic Substances and Disease Registry indicates that dioxin emissions turned upwards in the 1940's.19
Section 2.b: The years when human intakes of PCBs and dioxins were increasing:
Aside from emissions that are in close proximity to people (as from backyard burning), atmospheric emissions of PCBs and dioxins are only a first stage in the path towards harmful exposures to those chemicals for most people; according to the EPA, most human intake of dioxins and PCBs is via food, mainly meat, fish and dairy products; these foods would be from animals and fish that had consumed food grown where PCBs and dioxins had been deposited.20 So there would have been a lag between the beginnings of major increases of atmospheric emissions of dioxins and PCBs in the late 1940's and the time when most humans would be exposed to major increased intakes. Relevant information about actual human intakes is available from an EPA study of dioxin and PCB levels in preserved food samples from various decades going back to the beginning of the twentieth century;21.it was found that meat samples from the 1950s through the 1970s had concentrations that were 2-3 times higher for the dioxin TEQs (toxic equivalencies) and about 10 times higher for the PCB TEQs, as compared to current meat concentrations; this summary of that study's findings was as stated in a 2003 document by a committee of the U.S. Institute of Medicine.22 The above study was the only one mentioned in the above publication regarding exposures of Americans to dioxins and PCBs according to past time periods. A publication of the U.S. National Academies Press also refers to the 1950's through the 1970's as a high period for dioxin and PCB exposure.23
So it appears that, in addition to inhalation of dioxin emissions from rural backyard burning beginning in the late 1940's, harmful exposures of Americans to PCBs and dioxins in food would have begun in the 1950's; it probably would have been the early 1950’s, since it would probably take only very few years for atmospheric emissions from the late 1940's to become substantially incorporated into human food. Additional to the above would have been exposures to PCBs via inhalation of and dermal contact with PCBs due to their widespread uses in construction, transformers and other products during the 1950’s through the 1970’s.
Section 2.c: Development as a stage of special vulnerability to chemicals such as PCBs and dioxins:
Exposures to toxins during early childhood have been increasingly recognized to have major effects on health outcomes later in life. A team of 13 authors with the EPA, the NIH, and several U.S. and U.K. universities wrote a 2012 review article in which they generalized, "Chemicals and other environmental agents appear to have the ability to miscue the developing organism, resulting in maladaptation associated with increased disease."24 According to the World Health Organization, "many adverse environmental exposures such as to chemicals during childhood lead to disease or early death at adult age."25 An authoritative team of researchers (who are authors or co-authors of over 1300 articles and studies among them) wrote in 2012 that early development in utero and "during the first years of postnatal life" is "particularly sensitive to developmental disruption by nutritional factors or environmental chemical exposures;" they indicated that low doses could have developmentally disruptive effects; and they pointed out that early chemical exposures could lead to functional changes that "result in changed susceptibility to non-communicable diseases that will likely show up later in life."25a
Relevant information on this topic is also provided in The Faroes Statement, which was by 23 authors from around the world, many of whom were highly-published experts; this statement was an outcome of a conference sponsored by seven health- and environment-related agencies of the U.S. and European governments and WHO. Those authors were highly concerned about the special "susceptibility of early development" to environmental toxins; they referred to the "foetus and small child as highly vulnerable populations," which they said deserve extra protection from toxic exposures to environmental chemicals. They also said that chemical exposures during early postnatal life may predispose to disease during adolescence and adult life. The authors were especially concerned about long-term effects of "hormonally active substances (endocrine disruptors)," which they said might lead to increased disorders such as diabetes and cancer in later life. Of the few specific chemicals about which they expressed concern, polychlorinated biphenyls (PCBs) were said to be "highly immunotoxic." They also stated that "greater susceptibility to infections may be linked to prenatal or early postnatal chemical exposures."26
The reader should be sure to notice above the expert recognitions of
-- early postnatal toxic exposures as being on a par with prenatal exposures as hazards to development, as well as
-- development of the "foetus and small child" as being highly vulnerable to environmental toxins.
The above recognitions are especially important in light of the popular belief that only prenatal exposures to toxins are sufficiently significant to justify major concern about long-term effects. There is considerable other authoritative support for the serious significance of early postnatal exposures. (see Section 2 of www.pollution-effects.info)
Section 2.d: PCBs and dioxins: Many serious effects, especially in the long term:
Developmental exposures to PCBs and dioxins at levels at or near background levels have been found to have the following effects, which would have especially great consequences in the long term:
-- Toxicity to the immune system:
Remember from the Faroes Statement earlier the authoritative recognition of the "highly immunotoxic" effects of PCBs. Dioxins, also, have proven to be immunotoxic, according to highly-published scientists with the EPA and the NIH.30,43c According to the ATSDR, early postnatal exposures to PCBs may have profound effects on the immune system (as well as on the brain and thyroid gland), because of the related development that is ongoing at that early life stage.29
-- Damage to the blood-brain-barrier: In a 2009 study (Seelbach et al.),31 mice were administered PCBs in doses that resulted in a plasma PCB level that is comparable to the levels found in some human populations that have received brief exposures to PCBs.32 Shown in this chart is disruption of the blood brain barrier by three types of PCBs administered in that study: The right-hand three bars represent measures of permeability of the blood brain barriers of the PCB-dosed test animals, compared with permeability in the control animals that received only the vehicle (represented by bar on far left). Other studies provide additional evidence of the harmful effect of PCBs on the blood-brain-barrier.33
Multiple studies have found PCB exposures to be associated with liver cancer as well as other cancers,34 and PCBs are classified by the IARC as carcinogens and by the EPA as probable carcinogens. Dioxins are known carcinogens.
-- Endocrine (hormone) disruption:
According to the ATSDR, "Depending on dose and duration, PCBs can disrupt the production and disposition of thyroid hormones at a variety of levels;"35 and also, "it is agreed that the potential exists for these compounds (PCBs) to affect the synthesis, secretion, transport, binding, action, or elimination of natural hormones in the body...."36 Dioxins, also, have been found to have adverse hormonal effects,37 which will be dealt with later in the discussion of increasing suicide.
-- Major reduction of activity, which is important to mental as well as physical health:
According to the authors of the study that was the source of this chart (Jacobson et al.40), reduced activity was found to be associated with the PCB body burdens of 4-year-old children. The most-exposed children were found to be ”about 2-3 times more likely to be rated 'usually quiet and inactive,' and less than half as likely to be 'in action during much of the period of observation.' " The children who were observed were mostly from Great Lakes fish-eating populations, with slightly above-average PCB exposures.41 Notice the dose-response pattern, which is considered to be especially convincing evidence of causation.
So these were fairly typical environmental exposures, not poisonings, that appeared to cause the reduction of activity.
Reduced activity was also associated with postnatal PCB exposure in a Dutch cohort.41a At least four laboratory experiments have also found activity to be reduced by PCB exposure -- often greatly reduced; one of the experiments was by a team of researchers who said that the concentrations of the toxins found in their test animals' brains were "about the same order of magnitude as observed in (human) infants less than 1 year old."42
As indication of the relevance of the above to our discussion of long-term health effects of PCBs: according to a professor at Harvard Medical School, physical activity has been shown to help maintain a healthy body weight as well as promote psychological well-being, reduce the risk of various diseases including cancer, and "add years to our life.".43
Other long-term effects of dioxins include developmental toxicity, neurotoxicity, toxicity to the liver, gonadal atrophy, cardiovascular toxicity, and gender-related behaviors and may include porphyria, endometriosis, and reduced testosterone.43c
For further discussion of effects of PCBs and dioxins, see Section 6.
Section 3: The basic pattern of death-rate increases in relation to post-1950 increases in PCBs and dioxins
Section 3.a: This pattern as seen in recent years:
Fig. 2 repeated
We should consider how the above discussion about long-term effects of PCBs and dioxins relates to the pattern shown in Figure 2 earlier (repeated here). Remember that substantial intake by Americans of the rapidly increasing emissions of PCBs and dioxins started only in the 1950's. (Section 2a) Because of that, people in the 65-and-older age range would not have been exposed during their vulnerable infancies to the greatly increased PCBs and dioxins that began after 1950; observe the declines in death rates among all of those oldest age groups.
See how that contrasts with the increases in death rates that have occurred among people (below age 65) born after PCBs and dioxins started becoming widely present in the U.S. environment. (The 45-54 group will be discussed separately.)
Regarding the youngest children: The effects of background exposures to PCBs and dioxins appear to be life-threatening only in the long term; this is a reasonable explanation for the continued declines in death rates among the youngest children, as shown in this chart, even though they were born in the era of high PCBs and dioxins.
Section 3.b: Looking at a larger dataset and seeing the same pattern:
The charts examined above showed data for only six years (the latest six-year period for which data is available, as of the writing of this article); so a fuller set of data would permit a better understanding of what is happening, and such data is provided in the chart below.
(Source of data above from Table 5 at https://www.cdc.gov/nchs/data/nvsr/nvsr66/nvsr66_06.pdf
A fairly distinct transition from declining death rates to increasing death rates:
Looking at the figures above, going from right to left, from the oldest age groups toward the youngest, one can see a major transition taking place, from fairly consistent declines in death rates among people born in earlier years to many multi-year increases in death rates among middle-aged and younger people. (The point of transition is marked by "A," and subsequent multi-year increases in death rates are marked by B, C, and D.)
In all age groups between 15 and 64, only one (the 45-54 group) failed to show a multi-year increase in death rates; but that group's death-rate decline became notably halting and minimal in recent years and was therefore a minor but significant part of the changed picture after the transition at A.
Not shown in the above chart are continued declines that took place in death rates among children, in the youngest age groups. That completes a demonstration, in this larger data set, of the same pattern of death rates that was seen earlier in Figure 1: Increases in the central age range, while declines continued in the oldest and youngest age groups. If we can find a possible cause of deaths that is compatible with such a pattern, that could help identify the cause of the increased deaths.
To help understand what might underlie the increases in death rates, we should first remember the discussion of the vulnerability of early childhood development to environmental toxins, which may have long-term effects that could become apparent in adulthood. (See Section 2.c) Given the authoritative recognition of effects of early chemical exposures on adult health outcomes, it is reasonable to suggest the following:
If adverse health outcomes are observed for certain age groups of people in specific years, we should look for any increases in harmful chemical exposures that may have taken place during the early, vulnerable stages of those people's developmental periods. Therefore we should subtract those groups' average ages from the years of observed adverse outcomes, to see which early years should be investigated for possible increases in harmful exposures during early development.
Looking at the years that are marked in Figure 5 above: The 55-64 age group during the years marked at "A" would on average have been born 60 years earlier, in the early 1950's. So data indicates the early 1950's as the time of transition from birth years of people with consistently declining death rates (the older groups, on the right in Figure 5) going over to birth years of people with mainly increasing death rates (middle-aged and young people, represented at A, B, C, and D on the left).
Then remember (from earlier) that the 1950's were when Americans were determined to have begun consuming food with rapidly increasing contents of PCBs and dioxins. And remember also (from Section 2.d) that those toxins are known to have serious long-term health effects.
Consider whether exposures to those toxins in doses exceeding established safe levels by scores to hundreds of times (to be discussed later, at Figure 7 and accompanying text) at a developmentally vulnerable life stage could help explain the transition to earlier deaths.
Section 4: Exposures of developing children to PCBs and dioxins have increased, even though the toxins have been declining in the general environment, as seen with a close look at the exposures.
At first glance, there appears to be a major limitation to believing that PCB and dioxin exposures may have led to the increased death rates in the 21st century, at least as applied to death rates among younger people: both of those toxins started declining in the environment decades ago.
Section 4.a: Exposures of vulnerable, developing infants to the toxins may differ from and matter much more than presence of the toxins in the general environment.
PCBs were banned from most uses in the U.S. in the late 1970's, and dioxin emissions have been greatly reduced in recent decades as a result of regulatory efforts. However, both of these toxins are considered to be "persistent" for good reason, they are still emitted in vehicular45 and backyard burning pollution (see earlier), PCBs are still present in old products or buildings made or coated with them, and both are still present at hazardous levels in U.S. (and other) environments.46
So these toxins are still affecting people. But they have declined rather than increased in recent decades, and it may seem that they should therefore have had less effect on death rates in recent years. But death rates have nevertheless increased among the central-age groups. So it is reasonable to look farther. As it turns out, something has caused infant exposures to these toxins, at developmentally vulnerable times, to increase even though the toxins themselves have not been increasing in the overall environment.
A study in Taiwan found relevant adverse effects among children who lived in the vicinities of municipal incinerators; both gross and fine motor as well as other abilities were observed to be significantly reduced among many of those children, compared with children in the general population. As the researchers pointed out regarding those findings, emissions from incinerators are known to be important sources of PCBs and dioxins.44 However, substantial adverse effects were found only among the group of children who had been breastfed for at least six months; according to multiple authoritative sources, breastfeeding concentrates lipophilic (fat-loving) chemicals such as PCBs and dioxins in fatty tissues of mothers and transfers them to infants in doses scores of times higher than the doses received by the mothers.47
This same pattern was illustrated in another study that followed up on accidental exposures to dioxins in Seveso, Italy. A 2011 study (by Mocarelli and 12 others)48 of the aftermath of that accident measured characteristics of sons of mothers who had been exposed to increased levels of dioxins before their sons’ births, resulting in what the authors called “modest elevations” of the mothers’ dioxin levels. When the sons’ sperm quality and hormone concentrations were examined at ages 18 to 26, those who had been breastfed (and only those who had been breastfed) showed seriously adverse effects in all of the four different reproduction-related areas that were measured; by contrast, those who had not been breastfed showed no effects of the environmental exposures.
Both of the above studies strongly suggest that environmental exposures to lipophilic toxins, which can and do occur in modern industrial societies, can either have or not have harmful effects on developing children depending on the feeding type received during infancy.
Section 4.b: What it is that seems to determine higher versus lower exposures to PCBs and dioxins during the vulnerable developmental period:
As indicated in the study that was the source of the charts on the left, and in many other studies,48a exposures of developing children to lipophilic toxins (such as PCBs and dioxins) are very much determined by infant feeding type as well as by duration of any breastfeeding. U.S. studies from 2002 and 2007 show a similar pattern for infant exposures to dioxins specifically.49
Two experts on child development reported in 2006 that “Persistent lipophilic substances... such as PCBs (and dioxins), accumulate in maternal adipose tissue and are passed on to the infant in breast milk, resulting in infant exposure that exceeds the mother’s own exposure by 100-fold on the basis of bodyweight.”47 (italics added)
Breastfeeding would normally be the only source of high levels of those toxins in developing infants; the EPA, USDA and European researchers point out that over 90% of typical human exposures to both dioxins and PCBs is from food consumed, mainly from animal fats in food.50 However, observe in Figure 7 on left and in Figure 7a just below that scientists consider exposures to PCBs and dioxins via infant formula to be negligible.
(Below) Exposures of developing infants to dioxins, also, depend on feeding type:
PCB levels have been determined to be high in breastfed children well into the childhood years, as determined in a 1997 study in which PCB levels were actually measured at age 3.5 rather than merely estimated. (see Figure 7b below)
It appears that levels of PCBs in breastfed children continue for many years to be several times as high as the levels in formula-fed children, at least as determined in this 1997 Dutch study.
High levels of dioxins, also, can continue far past infancy in breastfed children, as determined in a study by a senior scientist with the EPA51 and as measured in breastfed young men in whom dioxin levels were measured at ages 18 to 26.52
Section 4.c: Exposures that vastly exceed established safe levels: The American Academy of Pediatrics and the American Academy of Family Physicians, both of which strongly advocate breastfeeding, do not deny that PCBs and dioxins are transferred to infants via breastfeeding in quantities that far exceed established safe levels. In an August, 2018 letter to the AAP, the author of this article wrote the following, based on considerable evidence from authoritative sources, which were cited: "PCBs have been found to be present in human milk in doses 63 to 270 times the minimal risk level established by the U.S. Agency for Toxic Substances and Disease Registry.4,6 Dioxins have been found to be present in typical U.S. human milk in concentrations exceeding the EPA’s RfD (estimated reasonably safe dose) by scores to hundreds of times.5,6 PCBs have been found to have long-term effects including cancer7,9 and damage to the blood-brain barrier; 8 dioxins have been found to have long-term effects including cancer, heart disease, reproductive abnormalities, and immunity deficits.9,10 "
The letter requested a response from the AAP that would contradict the above based on peer-reviewed scientific evidence, and offered $5,000 to compensate for the time required to write a response. (The financial offer was due to the lack of response to several earlier, similar letters to both the AAP and the American Academy of Family Physicians.) Return receipt for the letter was requested and received from the U.S. Postal Service, and (despite offer to place the funds in escrow to assure payment upon receipt of reply) as of over five months later, no response has been received. Any organization that promotes breastfeeding (such as the AAP) should have responded if the statements quoted above were not well-substantiated or if there existed scientific evidence that contradicted the substance of the letter that was received.
Likewise, there has been no reply to a similar letter to the AAP (dated Oct. 5, 2018) with similar financial offer to compensate for a science-based, contradictory response, stating, "Of toxins with recognized long-term effects, none are known to be ingested or inhaled by U.S. infants in doses beyond established safe levels, except for toxins that are transferred via breast milk." Again, return receipt for the letter was received, and again (after over four months) there has been no response and no sign of disagreement with the statement in quotes.
So there appears to be good reason to consider breastfeeding to be a major pathway -- or perhaps the only significant pathway -- for transfers of PCBs and dioxins from the environment to infants in hazardous quantities. Remember from Section 2.c that infancy is a stage at which development is unusually vulnerable to effects of environmental toxins. Given that, it is logical to look into the changing history of breastfeeding in the U.S., to see how that might relate to the recent increases in death rates.
Section 4.d: Historical changes in breastfeeding in the U.S.:
Shown below are charts indicating U.S. breastfeeding rates for past years going back to 1970.
Note above the major long-term increase in breastfeeding that has taken place since about 1971, according to the U.S. Surgeon General. Regarding continued increases of breastfeeding beyond the last data points shown above, see reference #63. For information about somewhat lower levels of breastfeeding in the 1960’s, with gradual increases beginning around mid-decade, see Section 5.b.
Also note on the left that there was a profound increase in breastfeeding for at least 12 months that was apparently underway as of 1980. 1980 was the first year for which 12-month breastfeeding data was provided by the CDC, or available anywhere apparently, so it is unknown whether 1980 was the first year of the increase; it might have started somewhat earlier, although there was very little remaining distance below 4.5% to allow for a significantly lower earlier starting level.
(A source of this chart currently at http://www.idph.iowa.gov/Portals/1/Files/WIC/2011%20national%20PedNSS%20data.pdf , pp. 35-37)
But even if the major upturn might have started before 1980, it is apparent that breastfeeding for at least 12 months more than doubled within a very short period, 1980-1982.
Huge increase in exclusiveness of breastfeeding: Finally, we should consider the significance of a major increase in intensiveness of breastfeeding, which would have taken place when exclusive breastfeeding came into being as a goal for many mothers. A well-published American expert on breastfeeding has pointed out that, as of 1992, "there probably were virtually no infants exclusively breastfed continuously from birth to six months of age;"53 but that was apparently to change soon. At about that time, the Baby-friendly initiative (launched in 1991) was coming into being as a major force, promoting adoption of practices at the center of which was exclusive breastfeeding. One of the expected "Ten Steps" for hospitals in this program is to "give newborn infants no food or drink other than breastmilk, unless medically indicated."54 The only outcome to which WHO points as evidence of the Baby-friendly initiative's "proven impact" is "increasing the likelihood of babies being exclusively breastfed for the first six months."55 There appears to be no consistent data available for exclusive breastfeeding rates in the 1990's;56 so it seems reasonable to use the data below about increases in Baby-friendly facilities as an indication of the time trend of exclusive breastfeeding.
Note in the above chart from UNICEF that the approximate years of the beginning of greatly-increased progress of the Baby-friendly initiative appear to be 1993-94. Although the U.S. Department of Health and Human Services didn't allow "Baby-friendly" designations until after a study was completed, hundreds of maternity facilities in the U.S. formally expressed intent to receive the Baby-friendly certifications in the early 1990's.57 In addition to the formal expressions of intent, according to a study published in 1995 but reporting on research carried out in 1993, "other, less formal efforts (were) underway at hospitals throughout the United States to implement the Ten Steps." 57 As mentioned, those Ten Steps include an expectation to breastfeed exclusively unless medically indicated to the contrary, and the successful impact of the Initiative promoting those Ten Steps was considered to be demonstrated by increases in exclusive breastfeeding. So an upsurge in intensiveness of breastfeeding -- and any effects that such an upsurge might have -- should have been expected to begin around 1993-94.
The total effect of all of the increases discussed above, combined with the known persistence of these toxins in the environment, would mean that transfers of PCBs and dioxins to infants were greatly increasing in recent decades, even though those toxins have been declining in the overall environment.
Increases in death rates in relation to increases in developmental exposures to PCBs and dioxins:
It would be worth looking again at the chart with data from the CDC (repeated below) showing the period of multi-year increases in death rates. A transition at "A" was discussed earlier at Figure 5 and following text, pointing out that death rates started increasing for the people, born in the 1950's, whose vulnerable early-postnatal years occurred when PCBs and dioxins were first becoming prominent in the U.S. environment.
The transition (at A) to periods of increasing death rates followed decades of nothing but declines in death rates, which characterized the times before PCBs and dioxins came to be highly present in the environment.
The death rate increase shown at B (5.6%) has been followed in that same age group by subsequent additional increases of 6.7% and 1.6%, in 2016 and 2017.61 This indicates that death rates increased substantially among people born beginning in 1971, on average; that was determined by subtracting the 35-44 age group's average age of 40 from the 2011 year of the beginning of the major increase in death rate shown at B.
So, making careful note of the content italicized just above, we should then look again at Figure 8 showing major increases in breastfeeding that began right after 1970, as well as at the section dealing with the levels of developmental toxins in typical human milk (Section 4.c). And then consider whether long-term effects (Section 2.d) of the increasing transfers of PCBs and dioxins via breastfeeding at that time could help explain the increasing death rates in the 35-44 age group, beginning in 2011.
Looking next at point C on the chart above, note the following: death rates increased substantially among people born on average in about 1981 and later; this was determined by subtracting the 25-34 age group's average age of 30 from the 2011 year of the beginning of the major increase shown at C.
So it is of interest to look back at the CDC data in Figure 9 above showing the more-than-doubling that occurred in breastfeeding for 12 months or more, taking place rapidly in 1980 to 1982, during the birth years of people whose death rates we see to be greatly increasing in later years.
The final increase in death rates in Figure 5 (repeated) above, for the 15-24 age group at D, had lasted for only two years as of the latest data on the chart. But that was already twice as long and the increase was several times as high (in %) as any increase that had ever taken place during several decades before the transition to worsened death rates among people born after 1950. And more importantly, recent data shows that the already very significant death rate increase shown at D was directly followed by an additional large increase of 7.8% in 2016, in that same age group.58
Again, it is worth a closer look at the probable origin of this increase. We should subtract the 20-year average age of this (15-24) age group from the 2014 year of the beginning of the death increases marked at D, to see that we need to focus on what was happening in 1994 and later; that would have been the average time of the vulnerable infancies of the people with increased death rates in 2014. In that regard, we should remember (from "Huge increase in intensiveness…" earlier In Section 4) the rapid increases of exclusive breastfeeding that were probably beginning in 1993-94; and then consider how much greater the effects of transferring PCBs and dioxins via breastfeeding could be if the infant is offered no other food or drink, other than breast milk.
As an indication of the magnitude of the transition to greater breastfeeding exposure that took place in about 1993-94, note that infant feeding advice published by the American Academy of Pediatrics in 1993 states that adequate intakes of "a commercial infant formula meet all the known nutritional requirements of an infant during the first six months of life" (p .25); essentially that same favorable statement about formula feeding is made elsewhere in that document (p. 13), and in neither case is anything said about any possible deficiencies or adverse consequences that might result from formula feeding.59 That was very different from the AAP's formally-expressed support for exclusive breastfeeding just four years later.60 So the dramatic increase in the movement toward exclusiveness of breastfeeding (Figure 10 and accompanying text), beginning in about 1993-94, would have taken off from a base at which feeding with formula would have been fully acceptable according to the highest U.S. medical authority specializing in child health. Also remember from earlier the expert statement about there probably being "virtually no infants exclusively breastfed continuously from birth to six months of age" as of 1992.53
As indication of the rapid increase that was about to start in 1993 in prevalence of exclusive breastfeeding, remember that, in about 1993-94, efforts were beginning "at hospitals throughout the United States" to implement the Ten Steps, which included exclusiveness of breastfeeding.57 So, if there could be long-term effects from exposures of developing infants to the high levels of PCBs and dioxins in human milk, such effects would be especially likely to have become apparent among people beginning to be born in about 1993-94. Note at D in Figure 5 (repeated) above that substantial increases in death rates did begin to show up in data for an age group (15-24) of people who, on average, were born in 1994 and later; the increases were especially large if one includes the additional 7.8% death rate increase that was recorded in 2016.
Reasons why exposures from decades earlier could be affecting death rates now:
It may seem to be unlikely that a change in infant feeding type long ago could be a significant factor in increasing death rates in later decades, especially when the change was toward more feeding of a type that is very widely believed to be beneficial. But there are good reasons to believe that substantial adverse effects, only recently observed, could be resulting from much earlier exposures. Remember that:
-- infancy is a stage at which development is unusually vulnerable to long-term effects of environmental toxins (see Section 2.c);
-- serious long-term adverse effects of PCBs and dioxins are well substantiated, by authoritative sources (see Section 2.d for details and most sources);.
-- both PCBs and dioxins in human milk have been found to exceed established safe levels by scores to hundreds of times -- a statement supported by ample authoritative evidence, and with which the American Academy of Pediatrics and the American Academy of Family Physicians have not disagreed (Section 4.c)
Although significant increases of PCBs and dioxins in the U.S. environment started in the early 1950's (Sections 2.a, 2.b and 3.b above), that was only the beginning of increases in human exposures. As discussed earlier (Section 4.d), there were major increases that later took place in transfers via the main pathway of those toxins to vulnerable infants, increases that have been irregular but ultimately very large over the years.
It should not be surprising that increasing average death rates have only recently emerged from the background, considering the slow-acting, long-term effects of PCBs and dioxins, the unevenness of the increases in infant exposures to those toxins, and the long-standing downward influences on overall death rates. The latter would have included the decline in smoking,43a the decline in the HIV/AIDS epidemic (in the 1990's), and life-extending results of normal medical advances.
So the recently-apparent average death rate increases, leading to declines in overall life expectancies, were probably merely emergence (from a contrary background) of outcomes that had been gradually developing over time.
Now that increases in death rates have become apparent, our attention ought to be drawn to any distinctive characteristics of the pattern of the increases – anything indicating that specific group(s) were more affected, or less affected, by the increases – which might help in determining underlying causes. See below.
Section 5: The age group that has shown notably favorable outcomes (the 45-54 age group) deserves additional attention:
Section 5.a: An exception to the death rate increases in the central age range: Remember from Figures 2 and 5 that the 45-54 age group was the sole exception to the three-part pattern that applies to the increases in all-cause death rates. Chronologically that age group was within the overall central-age range, subject to effects of developmental exposures to the toxins that became prominent in food in the 1950's, and old enough for long-term effects of those toxins to be felt; but the 45-54 age group seems to have come out well, compared with the increased death rates that have affected the rest of the individual age groups within that larger age range.
Another category in which that age group also stands out is that of deaths from drug overdoses involving opioids, a very major category, considering the opioid epidemic of recent years. (See chart below; there will be additional discussion of the opioid epidemic in Section 5.d.)
In the case of deaths connected with the opioid epidemic, the 45-54 age group again stands out as being far less affected than other groups in the central range.
In addition to its favored outcomes in the all-cause and opioid death rates categories, the 45-54 age group turned out to have had the most favorable outcomes also in two other important mortality categories: cancer and suicide, to be discussed in Sections 6.a and 6.c below.
So the 45-54 age group seems to have had exceptionally favorable outcomes in four distinct, important categories of death rates in recent years. When reflecting on that, we should bear in mind that
(a) PCBs and dioxins have several serious long-term health effects (see Section 2.d),
(b) infancy is a stage at which long-term development is unusually vulnerable to effects of such toxins (Section 2.c), and
(c) PCBs and dioxins are typically present at exceptionally high levels in human milk (see Section 4.c).
So it may be helpful to consider the various time periods during which developing infants would have had higher or lower exposures to PCBs and dioxins via human milk. It should be apparent that the 45-54 age group, with exceptionally low death rates in four separate important categories, was born at a time when breastfeeding was at an historically low level: the 1960’s (if discussing data from 2015-16). The next section will continue on this.
Section 5.b: The age group (45-54) that had the most favorable outcomes, born basically in the 1960's (see above)
Breastfeeding in the U.S. declined during the first six decades of the 20th century.53c,53d After a low period during the early-to-mid 1960’s,53a,53b gradual increases in extended breastfeeding (2-3 months or longer) followed;53a the turn came within a few years after the La Leche League published a book about breastfeeding in 1962, eventually selling over a million copies. (Only 17,000 of the earlier, unbound version had been sold.)53e A mid-1960’s time of transition is earlier than the sometimes-quoted 1971-72 turning point, which was apparently the average for any or one-week breastfeeding; but extended breastfeeding is more relevant to the health effects discussed here. Following the early gradual increases, there were major increases during the 1970’s and in later decades up to the most recent reports, although with irregularities in the overall upward trend. (Section 4.d)
Figure 2 repeated
Therefore people born in the 1960’s (the 45-54 age group, when discussing 2015-16 data) had lower exposures to PCBs and dioxins (see Section 4.c) during their critical developmental periods, in comparison with the more-breastfed age groups that came both before and after.
It would not be unreasonable to see a possible connection of the 45-54 group's reduced death rates with their reduced exposures to PCBs and dioxins during their developmental periods, especially considering how far such exposures can exceed established safe levels during a life stage of high long-term vulnerability.
Section 5.c: Are the recent death rate increases the new normal? There are good reasons to see them as such, with implication of a pressing need for appropriate response.
The pattern of death rate increases, shown above, appears to be unique in the history of death rates data provided by the CDC. As seen in the chart below, there have been only two other noteworthy periods of death rate increases since 1955, and each time only three age groups were affected. This time the affected population spans six decades, constituting an outstandingly adverse turn in death rates.
Above CDC chart from https://www.cdc.gov/nchs/data/nvsr/nvsr63/nvsr63_09.pdf
In both of the earlier periods of death rate increases (see just above), there were likely explanations for the increased deaths, factors that turned out to be impermanent (the war in Vietnam and the recreational drug culture during the 1960’s, and the HIV/AIDS epidemic during the 1980's). But this time the underlying causes might not be transitory. In the current case, it is apparent that the opioid epidemic contributes greatly to the deaths, but clamping down on legal sources of pain-relieving opioids appears to be merely turning much of the traffic toward illegal sources, leading to even more fatalities. (see Figure 11a below) There may well exist overall increased desires or needs for pain-relieving substances -- something recently new in the environment may have been leading to pain. This is a concern that should be addressed as a possible underlying cause of the epidemic.
Section 5.d: The opioid epidemic:
The opioid epidemic is a leading contributor to the recent increases in death rates. Between 1999 and 2017, more than 700,000 Americans died from a drug overdose.112 In 2017 alone, more than 70,000 people died from drug overdoses in the U.S.; of those deaths, about 68 percent involved a prescription or illicit opioid.113 A 2019 study in JAMA Network Open points out that the recent trend of major increases in opioid-related deaths will probably continue, despite efforts to restrict prescriptions.114
Above chart at https://www.nap.edu/resource/24781/Highlights_071317_Opioids.pdf
After 2011, when opioid prescriptions were reduced, deaths from illegal use increased dramatically (see above right).
The increasing opioid-related deaths during recent decades may have resulted from (a) increasing pain, leading to increased consumption of opioids (see below) and (b) low dopamine levels resulting from PCB exposures, leading to increased appeal of addictive substances. (see later)
Increasing pain and likely causes of that: According to a committee of the Institute of Medicine of the U.S. National Academies, the prevalence of chronic pain has been increasing.115 Aging of the population and better survival from diseases and injuries are partial explanations, but there other causes that should be of particular concern, including
-- the rising prevalence of obesity; and
-- low back pain (the most frequently reported pain condition), which increased from about 4% to over 10% of the population between 1992 and 2006; that is according to a study in North Carolina, providing data that the Institute’s committee says is compatible with national data from the Department of Veterans’ Affairs, (More about this below)
So it is of interest to review some recognized effects of the principal toxins discussed here.
PCBs, inactivity, and various causes of pain and deaths: Remember from Figure 4 and accompanying text about the effects of PCBs in reducing activity, which is clearly relevant to increase in obesity; obesity in turn leads to increased pain, including joint pain. Inactivity is also related to other pain- and mortality-related matters, including psychological well-being and risk of various diseases including cancer.43
Low back pain, dioxins and PCBs: Regarding this increasingly common, debilitating form of pain, note that dioxins have been found to reduce bone strength, particularly during development;116 related to that, micro-fractures in vertebrae, resulting from accidents and repeated stress, are associated with sciatica.117 And PCBs have been found to damage cartilage,118 the tissue that (when healthy) helps prevent sciatic/lumbar nerves from being stressed, as well as forming other pain-free joints. Also, reduced activity, a result of PCB exposure (Figure 4 and accompanying text), is contrary to the need for exercise and physical fitness that helps to prevent and deal with low back pain; weak back and abdominal muscles may not properly support the spine.119
Starting with painkillers, turning to heroin, and ending with overdose deaths: It seems to be authoritatively recognized that the especially rapidly-increasing deaths from heroin overdoses are largely end results of what started as use of prescription opioid painkillers, as indicated by the following: According to a publication of the U.S. National Academy of Sciences, following “national initiatives to reduce opioid prescribing… many people who otherwise would have been using prescription opioids (prescribed for pain relief) have transitioned to heroin use, with a resulting three-fold increase in heroin-involved overdose deaths from 2010 to 2014.”120 One can see a transition to heroin use taking place on the right side of Figure 11a above, with a rapid increase in opioid/heroin-overdose-related deaths continuing unabated at the end.
Blame for the opioid-related death increases has been attributed at least partly to relatively recent recommendations by governmental and organizational bodies, beginning about 1999, encouraging medical personnel to be more attentive to pain in patients; the view is that this has led to excessive prescribing of opioid painkillers, which in turn has resulted in the greatly increased overdose deaths. But subsequent restrictions on the prescribing of the painkillers have been followed by even greater overdose deaths, by means of greatly increased heroin use (see Figure 11a above).
Much data implies that something else – such as increasing pain in the population -- might be leading to increased use of the opioids. See below.
A statement from a committee of the U.S. Institute of Medicine referring to the increasing prevalence of chronic pain was mentioned above, followed by discussion of some likely causes of the increasing pain. An article in the American Journal of Medicine refers to “a new pain movement” and its impact on opioid prescribing.121 So it should not be surprising that (judging by the left-hand chart below) use of prescription opioid painkillers was already rising rapidly (in the early 1990’s) before the recommendations for greater medical attention to pain.
Above chart from https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0054496
As indicated both above and below, use of opioids in the U.S. population was already significantly increasing as of the early 1990’s. CDC data leads to a similar observation.122
(Above chart at https://www.jointcomd_History_Web_Version_05122017.pdfmission.org/assets/1/6/Pain_St)
Policies that would be expected to encourage prescribing of opioids did not start until after substantial, steady increases in opioid use were already ongoing. It was in 1998 that the Federation of State Medical Boards developed a model policy, subsequently widely adopted, that supported prescribing of opioids for pain management (p.144 of ref #115); the Veterans’ Administration first mandated the measurement of pain as the 5th Vital Sign in 1999;121 and it was in 2000 that the Joint Commission on Accreditation of Healthcare Organizations implemented standards with pain as the fifth vital sign.123
Therefore it should be of interest to explore whatever might have been contributing to the increases in pain that were already occurring as of the early 1990’s.
We should remember from Section 2.d that PCBs and dioxins are known to have long-term effects that can result in pain, including carcinogenicity, immunotoxicity, harm to the blood brain barrier, and reduction of activity; also remember from Section 2.c that exposures to toxins such as PCBs and dioxins during early development can have major consequences in adult life. Such things should be considered when problematic behaviors related to pain are observed. It is especially relevant that reduction of activity, which has been found to occur as a result of early exposure to PCBs, would reduce a natural, effective, very low-risk means of reducing pain; this will be discussed next.
Exercise (therefore physical activity) is a recognized leading means of dealing with pain, as discussed briefly earlier regarding low back pain. The CDC’s NCIPC Board of Scientific Counselors has studied alternative means of addressing patients’ pain problems without resorting to opioids; several non-opioid therapies for chronic pain were favorably mentioned by the scientific counselors or other experts at each of five separate places in a document on the subject; and in all of the favorable mentions, exercise or exercise therapy was the first alternative among several to be referred to.124 A publication of the National Academies Press states, “Exercise has been shown to be effective for treatment of many types and locations of pain,” citing 11 studies in support of that statement.125.
So exercise is clearly a leading (very possibly the best) means of reducing chronic pain without use of opioids. Anything that reduces a person’s innate inclination toward physical activity is likely to have adverse consequences for chronic pain, which is important since medical attempts at managing pain very often do not bring satisfactory results.126 Unsuccessful attempts at dealing with chronic pain might well lead people in the direction of non-prescription opioids, including heroin.
Fig. 4, repeated
Bearing in mind the above, remember the major reduction of activity that was found to be an effect, in a dose-response manner, of PCB exposures.41 Also remember the ways in which inactivity can lead to pain, by way of obesity (and joint pain) and risk of various diseases including cancer.43
Fig. 3 repeated
Disruption of blood-brain barrier by PCBs
(3 highest bars, below)
In addition to the pain-related long-term effects of PCBs and dioxins discussed above, we should remember also from Section 2.d the other long-term effects. Obviously cancer as well as other diseases (resulting from the immunotoxicity of those toxins) can cause chronic pain; and damage to the blood-brain barrier would probably allow entry into the brain of some of the many (sometimes harmful) chemicals that have come to be present in modern environments, very likely leading to painful headaches. Speed of pleasurable effects’ taking place via intakes of abused substances is very much affected by the blood brain barrier, and faster euphoric effects are associated with increased addictive potential of drugs.127
Statements from a 2008 review article on brain health are also of interest regarding the importance of an effective blood-brain barrier: “The brain is particularly sensitive to toxicity, because it is one of the most metabolically active tissues…. existing neurons do not divide and thus dysfunction or death of these cells may result in irreversible damage.”128 So any exposures (such as to PCBs) that have been found to disrupt the blood-brain barrier should be regarded very seriously, when considering what might have contributed to increasing levels of pain in recent decades.
PCBs, dopamine, and mental states:
Effects of PCBs in reducing the chemical, dopamine, in the brain are very relevant in relation to addiction. Dopamine plays a key role in the rewarding effects of alcohol and other substances; release of dopamine as a result of opioid intake leads to euphoria, according to the U.S. Surgeon General.129 Also, artificial (temporary) increase in dopamine transmission is reported to be the common effect of drugs of abuse that leads to addiction.130 Knowing the above, it is important to notice in the major document of the ATSDR on PCBs where it states, “the most consistent result from studies that examined the neurochemical effects of PCBs is a decrease in dopamine concentrations in different areas of the brain;” the authors cited nine studies in confirmation of that statement (including six that used relatively low doses of PCB in experiments with animals) and mentioned no studies conflicting with it.41b So we should consider possible serious drawbacks of the reduced dopamine concentrations that result from PCB exposures. See below.
A 2017 analysis of 31 studies (in JAMA Psychiatry) found basis for seeing a reduced level of dopamine as a state that may “create the cravings that may drive addiction.”131 Making a compatible observation but coming from the opposite direction, an experiment with monkeys indicated that higher levels of dopamine in the brain lead to significantly lower voluntary intakes of pleasure-inducing drugs.132 So exposures to PCBs, with their effect of reducing dopamine concentrations, could be expected to increase the likelihood of a person’s being excessively drawn to opioids.
Whereas exceptionally-high levels of dopamine lead to euphoria, normally-high levels lead to pleasurable feelings and enhanced mood.133 On the other hand, reduced dopamine levels (resulting from PCB exposures) may lead to
-- reduced habituation to pain, leading to increased intakes (and possible overdoses) of pain-relieving substances; the authors of a 2017 study stated that “several chronic pain pathologies… have been associated with dopaminergic deficits” (citing six studies as evidence);
-- cravings that could lead to addiction and overdoses (see above), and
-- lack of interest in life, inability to feel pleasure, feelings of hopelessness, and self-destructive behaviors,134 all of which are relevant to the recently increasing suicide rates (see Section 6.c),
We have not yet fully answered the question as to what may have led to increasing use of opioids as of the early 1990’s, whether as painkillers or to satisfy cravings. The chart below may be relevant:
(Above from https://www.nejm.org/doi/full/10.1056/nejmp1011512
93% of the overdose deaths were reported as involving opioids, in the one study from which this type of data was provided by the authors of the above study.135. Update on the above chart: the CDC reports that, as of 2017, overdose deaths from opioids had increased almost six times since 1999 136
As shown above, drug overdose deaths were not increasing for many years, before a gradual acceleration started. Remember that exposures to certain toxins during development can have major adverse effects in later life (Section 2.c); exposures to PCBs and dioxins can have long-term effects leading to pain (Section 2.d); and PCB exposures lead to reduced dopamine, likely increasing a person’s use of pain relievers and attraction to addictive substances (see “PCBs, dopamine and mental states” 5-6 paragraphs up); also remember that there were major transfers of PCBs and dioxins to infants (via breastfeeding – see Section 4.b) that increased gradually after about 1965 and rapidly after 1971 (Section 4.d).
Very few children are affected by opioid-related drug poisoning until at least age 15, as shown in CDC/ AHRQ data on the right; the numbers become much more significant beginning at about age 20. So any opioid-overdose-related deaths affected by increasing infant exposures to PCBs and dioxins would be very minor for many years, especially amid ongoing overdose deaths in the general population. But somewhere around 20 years after the beginning (around 1965) of increases in infant exposures to PCBs and dioxins, one might look for overdose-related long-term effects of the increases to start becoming observable. In line with that, we see (in Figure 11d above) deaths in the mid-1980’s for the first time beginning to rise above previously normal levels.
Then in subsequent years we should expect to see effects of greater percentages of the population having been born during a period of increasing infant exposures to PCBs and dioxins. See the right side of Figure 11d above.
Ethnicities in relation to heroin use and drug overdoses.
People are likely to think of such things largely with reference to inner-city minorities, and there used to be good reason for that impression. But that has changed. Observe in the chart below that, in recent decades, heroin use has become increasingly predominant among whites.
When observing the greatly increasing percentage of whites being involved in heroin use and drug overdoses, it may be relevant that whites have had far greater exposures to PCBs and dioxins during infancy, compared with blacks; remember the relationship between breastfeeding and exposures to PCBs and dioxins (Section 4.b), and then observe the differences in breastfeeding rates between whites and blacks; see below. (Note: The breastfeeding percentages shown below (for 1989) are lower than recent rates, especially for blacks, but they are much more representative of rates that would have prevailed when most children were being born whose adult outcomes are represented above.
To best understand how the comparative breastfeeding percentages would apply to effects of exposures to PCBs and dioxins over time, one needs to remember how much breastfeeding has increased since the 1960’s – see Section 4.d.
Pointing to increases in breastfeeding as a likely cause of the increasing deaths is clearly contrary to widely and strongly-held views about the benefits of breastfeeding. But the reader should notice that recognized effects of exposures to PCBs and dioxins, which are without question at very high levels in typical contemporary U.S. human milk (Section 4.c), fit well as likely causes of the increasing deaths, in various different ways.(Sections 2.c and 2.d) The rapid and even increasingly-rapid increases in deaths from opioid overdoses (see Figure 11a) are especially unusual for a non-communicable disorder; and such increases are compatible with a source of exposure that has been increasing (Section 4.d), and to which a progressively larger percentage of the population has been exposed through the years.
Given what is known about the long-term adverse effects of PCBs and dioxins (Section 2.d) and about the vulnerability of the early developmental period (Section 2.c), perhaps we should pay close attention to the fact that the (apparently healthier) 45-54 group was the least breastfed age group and therefore the least exposed to large doses of PCBs and dioxins during development.
Section 6: Other examples of PCB and dioxin exposures' being related to health outcomes, with more favorable results among the less-exposed (45-54) age group:
This section picks up on the topic of health effects of PCBs and dioxins, especially long-term effects, which were discussed earlier in Section 2.d.
Section 6.a: Cancer:
In the case of cancer, every age group above age 4 had declining death rates in recent data, probably largely due to the decline in smoking as well as advances in medical treatments. Note that the 45-54 age group, born on average in the 1960's, had the greatest decline of all, with more than twice the decline compared with all other age groups within the 25-64 age range.
(This table from https://www.cdc.gov/nchs/data/hus/2017/024.pdf)
Observing that death rates of children aged 0-4 were out of step with the rest of the population, and increased in this case, keep in mind that PCBs and dioxins could well be causal agents of this outcome again, since they are both carcinogens. Latencies in the case of childhood cancers can be very short; rapid cellular proliferation is taking place while children's bodies are growing, which probably affects the speed of cancer growth. Minimum latencies of certain childhood cancers have been determined to be 0.4 years, and others can be one year, based on National Academy of Sciences findings.62 Therefore the recent increases in deaths from childhood cancer might result from increased exposures of infants to PCBs and dioxins via human milk, in which those toxins are present in doses recognized to exceed established safe levels by scores to hundreds of times. (See earlier about PCBs and dioxins in human milk; see Figure 8 concerning increases in breastfeeding.). Having had less of those exposures during one's developmental period (which happened to the 45-54 group -- see Section 5) would tend to reduce cancer in mid-life, which might explain what happened with that age group. That could have been partly due to reduced exposures to carcinogens with long latencies, and partly due to reduced exposure to the immunity- and activity-reducing effects of PCBs and dioxins (see earlier); reduced activity is related to obesity, which has greatly increased in Americans in recent decades and is linked to cancer.
Apparently there is no other frequent pathway to infants, other than breastfeeding, for any carcinogen in doses that exceed established safe levels, not to mention two carcinogens, each far exceeding the safe levels. The American Academy of Pediatrics, a staunch advocate of breastfeeding, has not provided any response to contradict the above, even when offered good compensation for taking the time to do so. (see earlier) A December, 2018 search of the first eighty entries on Google Scholar (sorted by relevance) responding to the search phrase, "toxins to which people in U.S. are often exposed in excess of safe levels" did not bring up anything that met the requirements of that search phrase. Inquiries to the American Academy of Family Physicians and appropriate scientists also brought no responses that even attempted to answer a question about possible non-breastfeeding sources of carcinogens to infants.64
Section 6.b: Porphyria: A special reason why the increases in dioxin and PCB exposures after about 1950 would have been likely to increase deaths:
The toxic properties of PCBs and dioxins, discussed earlier, would have been in reference to the effects of each of those chemicals when assessed separately. However, those two toxins are normally both present in people at the same time; and their combined effects can be far greater still, compared with the already substantial risks when considered separately. According to the former chairman of the Canadian Institute of Child Health, the combined (synergistic) effects of toxins such as PCBs and dioxins are likely to be "more than multiplicative." He noted that a dose of PCB that alone will cause a 1.5 times increase in hepatic porphyrins will, in the presence of dioxin at a dose that alone produces no measurable effect, result in a 650-fold porphyrin increase.69e So we need to understand the effects of greatly increased porphyrins in the body.
The "overproduction disease" that is characterized by excess porphyrins is porphyria.69g According to a 2011 review article in the Journal of Clinical Neuroscience, accumulation of porphyrins can lead to "abdominal pain, neuropsychiatric symptoms and neuropathy."69f The Mayo Clinic says that people with neuropathy generally describe the resulting pain as stabbing, burning, throbbing, freezing, etc.;69h and symptoms of porphyria may include "vomiting,...paralysis,... confusion, hallucinations,...seizures;" complications include chronic pain, chronic kidney failure and liver damage. One common symptom is "sensitivity to the sun ... causing burning pain."69k Such symptoms and conditions could make continuation of life unpleasant for anyone, but burning pain resulting from sun exposure could make life especially hard to bear for farm people. Depression and psychosis, both of which greatly increase risk of suicide,69m,69n "occur often" in porphyria cases.69g And the disease "can't be cured," all that can be done is to try to manage it, by means such as avoiding sunlight,69k which may be unfeasible for people in many fields of work, especially in rural areas. Mortality is significant: 6 out of 47 patients as reported in one study,69o and 10 out of 25 in another study.69g
According to a UK research team, not only does porphyria have "potentially devastating sequalae," but diagnosis is "often overlooked."69p One implication of the above and of another article69g is that many deaths, very likely including suicides, may be resulting from porphyria without that disease being reported as a cause.
So increased death rates may well have resulted from effects of the increasing exposures to both PCBs and dioxins, as described above, which began in the late 1940's/early 1950's; those exposures, with their effect of dramatically increasing porphyrins in the body, could well have led to major pain, devastating consequences, and possible suicides, as well as to increasing involuntary deaths.
Section 6.c: Death rates from suicide in recent years are also reason for serious concern. Even though the actual numbers of suicide deaths may seem small, one should bear in mind that (according to CDC data), for every suicide attempt that leads to death, over 30 people attempt suicide; and an estimated 2.7 million Americans made a suicide plan in 2015 alone;65 all of this indicates serious distress among a very large number of people, such that the completed suicides are only the tip of the iceberg.
Fig. 13 (Source at https://www.cdc.gov/nchs/data/hus/2017/030.pdf)
Death rates from suicide appear to have been increasing in all age groups, but it is conspicuous that the adverse trend among the 45-54 age group (born on average in the 1960's) has been negligible while that of all other age groups has been substantial.
Bear in mind that the age group born in the 1960's would have had minimal exposures to PCBs and dioxins during their developmental periods (see Section 5). To understand why that should have reduced feelings that could lead to suicide, we need to consider the well-established long-term adverse effects of developmental exposures to PCBs and dioxins. The evidence on that topic is too lengthy to allow inclusion here, so that can be found in Appendix B.
The disproportionately rural incidence of suicide in recent decades provides additional evidence to support the hypothesis of dioxins as a cause of the increases in suicides. Again, the material on this topic is too extensive to permit inclusion here, so it has been placed in Appendix C. Basically, it points out that backyard burning of trash is basically a rural practice; and that practice is, according to the EPA, a very major source of emissions of dioxins. And that is a major source of dioxins to which rural people are exposed at close range. Dioxin emissions via this practice would have dramatically increased after plastics (which emit dioxins when burned) increased tremendously in the waste stream in the late 1940's. The time of that development was very compatible with the new predominantly rural prevalence of suicide that came to be at around that same time. See Appendix C for more.
Section 7: Additional matters:
Developmental exposures to dioxins and PCBs compared with calculated safe levels
(Above from study at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5225187)
Update on the basis for the calculated safe levels shown above (dashed vertical red lines): In 2001, the European Commission’s Scientific Committee on Food set a safe level for dioxins and dioxin-like PCBs that was similar to the level determined by WHO in 2001, which was the standard that was in effect during the WHO surveys, results of which are shown above.69s However, in November of 2018, the European Food Safety Authority (EFSA) issued a revised statement of tolerable intake, based on very substantial new evidence, that was seven times lower than that established in 2001 by its predecessor Committee.69t So the updated exceedances of tolerable intakes, according to the best currently-available evidence and research methods, are probably many times the exceedances shown in the charts above.
Prevailing belief in beneficial effects of breastfeeding, versus what has actually been happening:
There is clearly a general belief that breastfeeding is beneficial to the child, but whether that belief is based on good science and on recent data is a matter that should be explored. As discussed earlier, the author of this article has written letters to the American Academy of Pediatrics making statements related to the above and asking the AAP to try to contradict them with good evidence, offering ample financial contributions to compensate for the time required to write responses. Those statements, to which the AAP did not respond, included, "Essentially all of the studies that have found benefits of breastfeeding have been of the observational type, according to former Surgeon General Regina Benjamin.1 Leading authorities on medical evidence, including the chief editor of the American Medical Association’s Manual for Evidence-based Clinical Practice, as well as the doctor who is widely considered to have been the father of evidence-based medicine, have stated that evidence from observational studies is very predominantly of low quality.2,3 "
Observational studies find associations, such as would be found between high death rates in Florida and sunshine. Researchers normally feel that they can identify and properly deal with confounders (other, possibly actual, causes, such as the large elderly population in Florida); but they typically can't do that well, according to experts on medical evidence.73 Even if all confounders are recognized (which is often unlikely), it would be difficult for researchers to deal with confounders such as the greater likelihood of breastfeeding by women with good health habits; their children’s health would benefit from specific family membership,73b but the better outcomes would be attributed to breastfeeding, in typical studies.
Given the quality concerns about the evidence regarding advisability of breastfeeding, it makes sense to see what has actually happened during the decades when breastfeeding greatly increased in the U.S. As shown in a chart (Fig. 8) provided by the U.S. Surgeon General, breastfeeding rates in the U.S. have dramatically increased since the early 1970's, with breastfeeding for at least 6 months increasing about 10-fold since 1970. Other authoritative evidence indicates that breastfeeding actually started increasing, although relatively slowly, in 1965;70 but 1971 can be considered to be the starting point for major increases of breastfeeding in the U.S.
Obesity is one of the disorders said by the AAP to be reduced by breastfeeding,71 based on evidence that experts on medical evidence say is of low quality, a fact that the AAP does not dispute. (see earlier) So it is relevant to see what actually happened to child obesity in the years since breastfeeding greatly increased in the U.S. See below.
Above chart on p. 260 at https://www.epa.gov/sites/production/files/2015-06/documents/ace3_2013.pdf
When breastfeeding increased dramatically, child obesity also increased greatly. The same is true for diabetes and allergies. (see below)
The EPA document that is the source of the above chart also includes charts showing similar upward trends for ADHD (p. 246) and autism (p. 250), with the difference that both of those charts began at 1997 (although the increases started earlier).
It should be of no surprise that the above report of what actually happened historically in obesity prevalence aligns well with what was found in a large study of over 17,000 children followed from birth to age 16. That study (carried out by four PhD's and four MD's) incorporated randomization of breastfeeding promotion;72 randomization helps avoid the confounding that is inevitably present in observational studies.
Since the AAP also alleges that diabetes is reduced by breastfeeding, that is another area that justifies a close look as to what has actually happened historically while breastfeeding has been greatly increasing. According to the president of the American Diabetes Association, as of 2002 type 2 diabetes had "changed from a disease of our grandparents and parents to a disease of our children." At that time it was on its way to being what she called a "new epidemic" among children and young adults.74 According to the only readily-found study on the history of the increase of childhood diabetes, "the rising incidence of the condition was not widely recognized until the 1980s;"75 and the first reference found by the author of this article (after substantial search) to inclusion of young adults within this epidemic was in 2002. All of this points toward major increases in childhood diabetes coming some time after the start of the major increases in breastfeeding that began in the early 1970's. (For much more on this topic, see www.breastfeeding-and-diabetes.info.)
The AAP, when providing evidence to support its "conclusion that breastfeeding and human milk are the reference normative standards for infant feeding and nutrition," indicates allergic disease as another disease that they consider to be decreased by breastfeeding. In relation to that, it is relevant to see what actually happened with major types of allergies in the 2000's.
If breastfeeding were to have an effect of reducing allergic disease, we should expect to see evidence of that in data for the 2000's. But what we instead see (in the chart above) following major increases in breastfeeding are major increases in allergic disease. Notice that very large increases in both food allergy and skin allergy are shown for every one of the individual age groups shown in this chart, without exception; remember from earlier that all of those age groups would have been exposed to the greatly increasing breastfeeding of the 1990's and later, especially in exclusiveness.
To summarize the preceding: The AAP publicizes that effects of breastfeeding include reduction of obesity, diabetes, and allergic disease, all of which is based on observational studies, the type of study that the highest authorities on medical evidence say essentially produces evidence of low quality; the AAP does not dispute this. And in the several decades during which breastfeeding greatly increased in both percentages and exclusivity, what has actually occurred has been dramatic increases in each of those diseases among children who would have received the increased breastfeeding.
Also of interest are changes that have occurred in important health areas not discussed by the AAP, during the years when breastfeeding was increasing greatly. Of particular interest are changes in child health data for after 2000, following exposures to breastfeeding that were greatly increasing in intensity (see earlier) as well as in percentages; the early 2000's are also the period for which the available health data is most complete.
The chart on the left is fairly self-explanatory, showing what has happened regarding the health of many American children who were infants during the 1990-2010 major increases in breastfeeding. (Increases in breastfeeding continued well after the data shown earlier in Figure 8.76)
In a separate study, published in the journal Pediatrics and reported by a team that included six doctoral degrees within the group, among U.S. children aged 0-17 there were the following major increases between 2001 and 2011:
-- disability associated with speech problems (63.1%),
-- mental retardation or intellectual impairment (63%), and
-- other mental, emotional, or behavioral problems (64.7%).77
For gathering their data, the researchers utilized "the only continuing nationwide survey" of U.S. health information, one that is conducted annually by the CDC's National Center for Health Statistics (NCHS) and which has been the principal source of information for the U.S. Department of Health and Human Services to monitor health trends in the United States since 1957. Note that the above very large health declines were all reported for just one decade, following major increases in breastfeeding exposures of the general population of children in which the health declines were observed. Also note that relevant increases in breastfeeding were not only as shown in Figure 8 but also as seen in Figure 10.
In Table 1 of the above study, it was reported that by far the greatest increases in childhood disability were among children of college graduates. That is pertinent to this discussion since, during the relevant years, exclusive breastfeeding rates of college graduates apparently increased 2-1/2 to 3 times as much as the equivalent rates of women with high school degrees or less.77b This would have resulted in much greater transfers of PCBs and dioxins to the developing infants of college graduates. (see Figure 7 and accompanying text)
Another outstanding figure in this study's data (also from its Table 1) was the increase in disability among children in two-parent families, at three times that of children of single parents. And over the relevant years, in another statistic that could be relevant, exclusive breastfeeding through six months apparently increased twice as much among married mothers as among unmarried mothers.77c
The AAP also discusses neurodevelopmental outcomes as an area showing presumed benefits of breastfeeding. Recent increases in neurodevelopmental impairments, following increases in breastfeeding, were discussed just above. It is also of interest to look back at the longer-term history of neurodevelopmental outcomes. A 2008 publication of the U.S. Center for National Health Statistics states as follows: “Over the past three decades in the United States, behavioral and learning disorders have emerged as major chronic conditions affecting the development of school-aged children and adolescents.” (This statement was based on observations of pediatricians and educators as well as government statistics.)78 A 2012 study by a team of scientists from the U.S., France, U.K., Denmark and New Zealand referred to the “many… major diseases – and dysfunctions – that have increased substantially in prevalence over the last 40 years;” their primary focus, regarding possible causal factors in the environment, was on the period of early development.79 It is easy to subtract decades of disease/dysfunction back from the publication years of the above statements, to see the 1970's as the beginning time for the seriously adverse trends in health. Remember the 1970's as the time when the rapid increases in breastfeeding began (Figure 8)
Health problems in the general population born since the 1970's:
U.S. military recruiting statistics from a 2009 publication indicate that the increasing health problems among Americans born in recent decades have affected most of the young population, not merely a minority.79a 27 percent of young Americans have in recent years been found to be too overweight to join the military; an additional 32 percent of U.S. young people have been found to have other health problems that prevent them from serving; and about 30 percent of potential recruits with a high school degree fail the Armed Forces Qualification Test of basic math and reading skills.79a Unfortunately there seem to be no published military statistics available from earlier generations to permit direct comparisons, but there are good reasons to consider the recent figures to be dramatic increases over figures from earlier decades; we can gain some insight based on
-- the data charted in Figure 15 earlier, showing a tripling of obesity that occurred among children aged 2-17 between the 1970's and recent years,
-- the major increases in mental, emotional, or behavioral problems that were found to have taken place in children between 2001 and 2011 (see above), and
-- the 63% increase in learning disability that occurred between 1987 and 2001.79b
So, if we look at what has actually happened with the physical and mental health of the young people born since U.S. breastfeeding started increasing greatly (beginning in the early 1970's), we see a picture of considerable health declines. It is worth remembering that the American Academy of Pediatrics does not dispute that the studies they cite as evidence in favor of breastfeeding are of the type (observational) that leading experts on medical evidence say provide predominantly low-quality evidence. (see earlier)
The unfavorable health developments among people born after the1960's are not part of a simple one-direction trend. As discussed in Section 5, death rates of Americans born in the 1960's have been distinctly favorable in comparison with those of people born in the previous decade also. Americans born in the 1960's appear to have been healthier than people born both before and after them. In relation to that, we need to remember that people born in the 1960’s were also the least-breastfed group, very possibly the least-breastfed group ever. (See Section 5.b)
Section 8: Other, more-recently widespread toxins (brominated flame retardants) that would have added to effects of PCBs and dioxins:
Other toxins that may have had effects similar to those of PCBs and dioxins, but which started increasing later than those other toxins, were brominated flame retardants. PBDEs are a major type of those chemicals that are “close cousins” of PCBs and are “very structurally similar” to one of the two major types of PCBs, according to M. M. Merzenich, who is a member of both the U.S. National Academy of Sciences and the Institute of Medicine.83 The EPA agrees about the structural similarity of PBDEs to PCBs.84 Dr. Merzenich brought up PBDEs when discussing an experiment with rats that he and colleagues carried out.85 According to him, seriously adverse effects on nursling rat pups’ brains, lasting into adulthood, were “achieved by feeding the rat mother just enough of the poison to match the levels of PCB recorded in nursing human mothers in high-PCB-exposure areas of the U.S.,” which he indicated to be "all over the country."86
Apparently considering PBDEs to be similar to PCBs both in their likely effects and in their prevalence in the U.S. environment, Dr. Merzenich concluded, “If human fetal and infant effects parallel rat impacts, we would predict that there would be a correlation between the PCB/PBDE levels in human breast milk — and in infant blood — with the probability of autism onset.”
There is good reason to believe that effects on human infants would parallel the effects observed in animals.87 According to a consensus statement signed by 57 scientists, researchers and health professionals, including many who are highly published experts, "The concordance between human and animal neurotoxicity assessment is remarkable as demonstrated for lead, mercury and PCBs."88 But there is also good basis to believe that animal studies greatly under-estimate the neurodevelopmental effects on humans, by 100-fold or more, according to a 2002 article (Stein et al.) by a research team that included three MD's.89
Knowing that PBDEs are authoritatively considered to be toxic equivalents of PCBs, note the following: PBDEs rapidly became widely present in environments and in human milk in industrialized countries during the final decades of the 20th century, reaching high levels.90 According to a 2007 report to the Maine legislature by an official of the Maine CDC, ”Several studies reported that levels of PBDEs in human tissues are now higher than PCBs, including in the U.S.;” in two out of 52 individuals in one study, PBDE levels were found to be 100 times greater than PCBs.90a
The increases of PBDEs in environments of developed countries occurred while declines were taking place in PCBs and dioxins in the environments during those same years.
Although this article has primarily dealt with likely causes of increased death rates, it is reasonable to broaden the discussion into ADHD and autism for the following reason: Increases of developmental exposures to PCBs and dioxins, as discussed earlier in this article (Sections 2.c and 2.d) can reasonably be seen to be a likely cause of the increased death rates; and breastfeeding is clearly the only major pathway for those toxins to developing infants, at an especially vulnerable life stage. But widespread, strongly-held belief in the value of breastfeeding will work against any reduction of that pathway as a source of exposure. Section 7 discussed some reasons why breastfeeding should not be so highly esteemed, but more can be said on that subject, especially now that the set of toxins of concern is seen to also include PBDEs.
The EPA discusses PBDEs' “adverse neurobehavioral effects following exposure during the postnatal period" and refers to neurobehavioral effects of PBDE exposures as being a “critical endpoint of concern.”91
Even the comparatively low exposures to PBDEs outside the U.S. appear to have been having adverse effects, as indicated by the following:
-- In a 2011 Spanish study it was found that exposure to mothers' elevated PBDE levels via breastfeeding (but not during gestation) had effects including an 80% increase in relative risk of attention-deficit problems and a 160% increased relative risk of poor social competence.92 (Note that “poor social competence” is a way of describing a basic characteristic of people with autism.)
-- Another Spanish study found “an association between PBDE concentrations in colostrum (early breast milk) and impaired infant cognitive development," with the effect being stronger with longer duration of breastfeeding.93
-- According to a study by four Taiwanese scientists, “Neonatal (relating to the first month after birth) exposure to BDE-209 (one type of PBDE) has been found to have developmental neurotoxicity, including hyperactivity; learning and memory defects;“94
-- A European study determined that levels of PBDEs in human milk as found in several European studies were many times higher than levels that should be considered safe;95
-- Another European study by a team of 15 researchers, published in 2016, determined a very high probability that PBDEs cause IQ Loss and Intellectual Disability.96
Bearing in mind the findings of the above European studies, note that PBDE levels in North America have been found to be 10 to 100 times those in Europe and Asia.97
Most of the above studies showed results broken down only into two or three large groups, with groups each containing large sections of the population.98 Narrower breakdowns would be likely to reveal far more serious effects at the highest exposure levels, since a U.S. study (Schecter et al.) found that PBDE levels in the top 5% of the population were 10 to 100 times the median levels.99
Above chart on p. 246 at https://www.epa.gov/sites/production/files/2015-06/documents/ace3_2013.pdf
While breastfeeding increased greatly, ADHD also increased greatly.
A 2013 U.S. study that was described by its authors as “the largest study to date on the potential neurodevelopmental impacts of PBDE exposures” arrived at relevant findings on this topic: it was found that increased PBDE level in a 7-year-old child was associated with a 4.5 times higher odds of the child being rated by the teacher as being in the “moderately or markedly atypical” range on the standard Hyperactive/Impulsive subscale, and with a 5.5 times higher risk of the child being rated as moderately or markedly atypical in the scale for Total mental disorders.100
The increase of toxins that was linked to the above increased risks was ten-fold, which sounds like a lot, but it isn’t when discussing PBDE exposures; remember that the difference between median PBDE exposures and exposures of the top 5% was found to be 10- to 100-fold.99
A good fit with the predominantly-male percentages of those affected by the recently-increasing neurological disorders and difficulties in education:
Some types of PBDEs have been found to inhibit production of testosterone,102 and testosterone is important to male neurological development.103
Although the study from which this chart was taken dealt with exposures to PCBs, we should remember the similarity between the structures and likely effects of PCBs and PBDEs.
The EPA points out that studies with rats and mice indicate that PBDEs have most of the same long-term effects as PCBs and dioxins – immunotoxicity, carcinogenicity, hormone (endocrine) toxicity, developmental neurotoxicity, liver toxicity, and other effects;104 and, considering the similarity of PBDEs to PCBs (see earlier) it is likely that they also have the other long-term effects as well.
Above from p. 250 at https://www.epa.gov/sites/production/files/2015-06/documents/ace3_2013.pdf
Part of the reported increase in autism is due to widened definition and increased identification of the disorder, but part of it is also considered to be real.
As mentioned earlier (beginning of Section 8), Dr. Merzenich saw a likely link between fetal and infant exposures to both PCBs and PBDEs, as measured in breast milk, and likelihood of autism diagnosis, based on research by him and his colleagues. There is also substantial other evidence of links between autism and this major pathway of PCBs and PBDEs to developing infants, some of which follows.
Autism, like the other disorders discussed above, is reported to have greatly increased in recent decades. As with the others, the increases have been far too rapid to be attributed to genetic changes, so we should look for anything relatively recently increased in the environment that could be responsible. As discussed earlier, people who ought to be knowledgeable do not seem to know about any widespread source of developmental toxins to children in doses exceeding established safe levels, other than breastfeeding; and they do not dispute that PCBs and dioxins are present in typical human milk in doses scores to hundreds of times the safe levels.
Studies that have found prevalence of autism or other neurological impairment to correlate with breastfeeding:
Many studies, mainly published in 2009 and later, have found positive correlations between breastfeeding duration and autism prevalence. One of those studies investigated data from all 50 U.S. states and 51 U.S. counties and found that "exclusive breast-feeding shows a direct epidemiological relationship to autism," and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism."105 A Canadian study investigated a population of over 125,000 and found breastfeeding (versus not breastfeeding), while still in the hospital, to be associated with a 25% increased risk of later diagnosis of autism.106 Another U.S. study found a 185% increase in autism among children who had been breastfed for at least six months, compared with controls, with a very high level of statistical significance.107
A 2015 study based on 902 ASD cases found a 47% greater risk of ASD among breastfed children than among controls.108 In a 2012 study, of 33 children who had been breastfed by mothers with above-average levels of PCBs, 9 had mental delay, whereas none of the 11 non-breastfed children with similar PCB exposures had mental delay.109
Another 2015 study found a 3% increase in odds of autism diagnosis for each additional month of any breastfeeding and a 4% increase for each additional month of exclusive breastfeeding, as well as a 30% increase in odds of autism with six months of exclusive breastfeeding versus no breastfeeding.110
The CHARGE study in California, the especially large SEED study (carried out at six different sites across the U.S.), and another important U.S. study have found that children later diagnosed with ASD or ADHD had been breastfed for average durations of 6.7, 7.3 and 5.9 months. By contrast, median durations of breastfeeding in the general U.S. population in the relevant years were found in all of the four large surveys to be about 3 months.111
Aside from neurological disorders, over 40 studies have found breastfeeding to be associated with greater prevalence of various diseases and adverse health outcomes. See www.breastfeeding-studies.info. Obviously, these studies are not mentioned by the promoters of breastfeeding.
It appears that the distinctive age-group profile of the recent death rates could be largely explainable according to the recognized long-term effects of PCBs and dioxins. (see Sections 2.c and 2.d) Those toxins greatly increased in the U.S. beginning not long before 1950 and increased in the U.S. food supply within a few years after that (Sections 2.a and 2.b); and exposures of developing infants to them greatly increased after 1971 (Section 4); and there have been many increases in death rates in specific age groups at certain times that are very compatible with long-term causation by PCBs and/or dioxins, to which vulnerable infants were exposed in increasing amounts at relevant times during development. (see Figure 5 repeated and text below it)
There have also been increases in physical and mental health impairments among children and young people in recent decades, which have apparently been higher among those groups that would have had the greatest exposures to PCBs and dioxins as infants. (Section 7)
Credibility of the causation suggested above: It is important to bear in mind that the implication of PCBs and dioxins as causal factors for deaths in later life is not based merely on existence of moderate exceedances of established safe levels, such as 50% or so; it is based on knowledge of infant exposures' exceeding safe levels by scores to hundreds of times; this is not disputed by people who ought to know about it. And those exposures occurred during a life stage authoritatively recognized to be especially vulnerable to toxins -- such as PCBs and dioxins -- that have long-term effects.
Should parents be informed of the reasons to doubt the advisability of breastfeeding, rather than hearing only strong recommendations from the authority figures to whom they are exposed?
1) On the basis of a type of evidence that highest authorities on medical evidence consider to be of low quality, the AAP strongly recommends that vulnerable, developing infants be fed a substance that includes extremely high levels of recognized developmental toxins. The AAP does not dispute the information included in this statement.
2) While promoting breastfeeding, the AAP withholds from parents undisputed information about the high levels of developmental toxins contained in human milk, and about the many studies that have found harmful effects of breastfeeding. Aside from the several studies that have found breastfeeding and duration of breastfeeding to be associated with autism and higher prevalence of autism (see Section__), there have been dozens of studies (including the gold-standard type -- randomized controlled trials) that have found other adverse effects of breastfeeding. (See www.breastfeeding-studies.info)
Appendix A: Burning of plastics as a major source of dioxin emissions in the environment:
Burning of plastics is known to release dioxins. Biemiller, Can we safely burn used plastic objects in a domestic fireplace? MIT School of Engineering, Ask an Engineer, at https://engineering.mit.edu/engage/ask-an-engineer/can-we-safely-burn-used-plastic-objects-in-a-domestic-fireplace/ The NIH points out that numerous household, medical and construction products and materials contain PVC plastic, which emits dioxins when burned. Tox Town: Polyvinyl Chloride (PVC), at https://toxtown.nlm.nih.gov/text_version/chemicals.php?id=84 Trash (beginning in the mid-20th century) would typically contain PVC plastics as well as coated paper. Household and farm burning of trash is common in rural and non-urban U.S. At the EPA "An Inventory of Sources...." listed above, see p. xliv and Section 6.5, "Backyard Barrel Burning."
-- New York Times: In Rural Areas, the Heat Is on Over Practice of Trash Burning, By Lisa W. Foderaro, MARCH 7, 2005 , at https://www.nytimes.com/2005/03/07/nyregion/in-rural-areas-the-heat-is-on-over-practice-of-trash-burning.html?pagewanted=all The EPA considers backyard barrel burning to be the largest quantifiable source of dioxin emissions in the U.S. as of the latest national inventory. EPA: An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000, especially Table 1-17 ofmpub.epa.gov/eims/eimscomm.getfile?p_download_id=523391 Compared with combustion in municipal incinerators, open burning typically takes place mainly in the lower end of the temperature range, where dioxins are most readily formed.
See also the sources at reference 16.
Appendix B: Well-established effects of PCBs and dioxins that are likely related to the increases in suicides:
(see earlier for most information sources)
-- Toxicity to immunity leaves one vulnerable to disease, as does exposure to carcinogens; diseases can be painful, physically harmful and/or disfiguring, and treatments for them can impoverish a person. All of those would diminish the likelihood of having a life that is pleasant to continue. Pain of disease can also lead to use and misuse of opioids, alcohol and other addictive/hazardous substances, which can lead to accidental or intentional overdoses, which have been increasing;
-- Damage to the blood brain barrier would leave the brain more vulnerable to the many toxins in contemporary environments, with unknown (but likely adverse) effects on what goes on inside the brain;
-- physical activity is known to promote psychological as well as physical well-being, and the effect of early exposures to PCBs in reducing activity would be adverse in those areas;
-- hormones are known to be important to moods, and the harmful effects of dioxins on endocrine glands would be likely to be significant in that area. It has been found in animal testing that lactational exposure to dioxins harms the pituitary gland,39 which produces hormones that control the hormonal balance in the body66 as well as production of sex hormones.67 (All males have some estrogen and all females have some testosterone, but in different proportions.) We should consider whether imbalances of sex hormones during the sex-characteristics-formative pubertal and teenage years, possibly resulting from dioxin's effect on the pituitary gland, could cause some individuals to have sexual orientations that don't fit in well with the general culture of which they are part, or with parents' strongly-held expectations. Some evidence has shown that environmentally relevant exposures to certain endocrine disrupting chemicals such as PCBs could affect brain sexualization.67a A 1998 study in the American Journal of Public Health found male bisexuality/homosexuality to be associated with a seven-fold increased odds of suicide attempt;68 a report of the U.S. Department of Health and Human Services stated that gay and lesbian youth were two to three times more likely to attempt suicide than other young people.69
The CDC states that "in men, lowered levels of testosterone have been associated with environmental and occupational exposures to dioxin-like chemicals" (which include major types of PCBs as well as dioxins), citing six studies in support of that statement, as well as pointing out that gonadal atrophy has been observed in animal studies of exposures to those chemicals.69d
It should be emphasized that effects of PCBs and dioxins, in italics above, are well substantiated, by authoritative sources (see Section 2.d for most sources). And we should remember that (a) PCBs and dioxins in human milk have been found to exceed established safe levels by scores to hundreds of times (a statement with which the American Academy of Pediatrics does not disagree -- see Figure 7 and accompanying text), and also (b) infancy is a stage at which development is unusually vulnerable to long-term effects of environmental toxins. (see Section 2.c)
In the case of suicide, death rates have also been increasing among the oldest age groups, not merely those born after 1950. That helps form a somewhat different picture of the health record of the least-breastfed age group (45-54, born in the 1960's): In this case, their outcomes were not only more favorable than those of all of the other central-age groups; in this important case, outcomes for the least-breastfed group were far more favorable than those of all other age groups for which the death rates are recorded. (see Figure 13)
In this chart showing figures for suicide deaths among 10-19-year-olds, notice the stable or slightly declining death rate during many years preceding an upturn in 2008, and the 56% increase that then took place between the low point and 2016. In the case of teen suicides (recently referred to as an epidemic), the significance in terms of distressed lives is especially understated by the numbers of actual suicides: for every completed suicide, as many as 400 teens report attempting suicide.69a
To determine the average birth year of the youths whose increasing suicide rates were at the beginning of the major increase, subtract the group's average age of 15 years from the year of the beginning of the long upturn (2008) to arrive at 1993. Then remember when exclusiveness of breastfeeding was apparently starting to increase dramatically (1993-94 -- see earlier); and consider the probable effects of greatly increased intensiveness and duration of breastfeeding in increasing transfers of dioxins to infants. (see earlier) Also remember about effects of dioxins on hormones that could be related to teenage suicide. (see earlier)
Appendix C: The disproportionately rural incidence of suicide in recent decades:
This provides additional evidence to support the hypothesis of dioxins as a cause of the increases in suicides.
According to a 2001 study by three Harvard University researchers, when comparing suicide rates according to urban-versus-rural locations, "the percentage of population living on farms positively predicts suicide."69b Public health officials and others have speculated as to the underlying causes of the high and increasing suicide rates among farm people, typically suggesting such factors as stagnant incomes, unpredictable weather conditions, rural isolation, lack of mental health services, etc., even though most of those conditions have always been part of farm life. And there is some evidence indicating that suicide prevention treatment has little or no impact on suicide-related behaviors anyway.69c Therefore consideration of other possible causes of the high and increasing rural suicide rates, other than those typically suggested, is in order.
Evidence implies that there has been a change in the environment since the mid-20th century that could account for the high rural suicide rates since that time: According to an in-depth history of suicide published in 1991, "Ever since statistics on suicide were first kept, researchers and reformers have suggested that the rate of suicide is lower in the country than in the city...;" the author then pointed to a reversal that had taken place in that generalization in recent decades. (His year of publication was 1991.)69q A 2002 study provides more precise information: judging by trend lines shown in that study, the increasingly-rural suicide trend was clearly already underway as of before the 1970 beginning of the study's data.69r
Changes in overall historical suicide rates could provide relevant clues. Those had been trending downward during the later decades that led up to the mid-1950's, at which time they turned upwards. (See below.)
We should remember (from earlier) that PCBs and dioxins greatly increased in the U.S. in the 1950's. In addition to long-term effects on developing children (discussed earlier), there would also have been faster-acting effects that could have made life unpleasant for some members of most age groups. (see earlier) Effects of dioxins, in particular, could be helpful in explaining increases of suicides in rural areas after about 1950:
a) Remember (from early) that production of plastics increased dramatically in the U.S. after World War II, which would have led to considerable burning of trash that contains plastics (a practice known to emit considerable dioxins), beginning in the late 1940's; such burning is well known to take place widely in rural but rarely in urban areas.
b) Backyard burning is currently considered by the EPA to be the largest known source of dioxins in the U.S., exceeding all of the many other major sources of such pollution.69u Many or most of the other major sources would normally be emitted from tall stacks, from which hot emissions would rise and continue rising and disperse greatly before falling back to earth. This would contrast with the concentrated, close-to-people emissions of dioxins from backyard burning.
Therefore there would have been major emissions of dioxins, at ground level, in rural areas beginning in the late 1940's; those close exposures may well largely explain the increases in rural suicide rates in recent decades.
For any increasing non-rural suicide rates in the 1950's, passage of the newly-increasing dioxin emissions up into the human food supply would almost certainly be a causal factor; this would be in line with the EPA's generalization that over 90% of typical human exposure to dioxins is via food, a generalization that would best apply where typical studies would be most likely to be carried out, near metropolitan areas.
1) The Surgeon General’s Call to Action to Support Breastfeeding 2011, p. 33, at www.surgeongeneral.gov/library/calls/breastfeeding/calltoactiontosupportbreastfeeding.pdf The Surgeon General stated, "research on the health outcomes of different modes of infant feeding is limited to observational studies."
2) Figure 2 in Guyatt et al., GRADE guidelines: 1. Introduction -- GRADE evidence profiles and summary of findings tables, Journal of Clinical Epidemiology, at http://www.jclinepi.com/article/S0895-4356(10)00330-6/pdf Dr. Gordon Guyatt is chief editor of Users' Guides to the Medical Literature: A Manual for Evidence-based Clinical Practice, 2nd Edition, copyright American Medical Association; 26 pages of this manual are devoted to examples of studies (almost all of which were observational) that were later refuted by high-quality studies.
3) Dr. David Sackett, writing in The Canadian Medical Association Journal, as quoted in “Do We Really Know What Makes Us Healthy?” New York Times, published: September 16, 2007 at http://www.nytimes.com/2007/09/16/magazine/16epidemiology-t.html?pagewanted=2&_r=0 Dr. Sackett's reputation: BMJ 2015;350:h2639, at https://www.bmj.com/content/350/bmj.h2639
4) Oregon Department of Environmental Quality Environmental Cleanup Program, Oct. 2010, 10-LQ-023, p. D2-4 (attachment 2 of Appendix D, near very end) at www.oregon.gov/deq/FilterDocs/HumanHealthRiskAssessmentGuidance.pdf
5) Lorber et al., Infant Exposure to Dioxin-like Compounds in Breast Milk, Vol. 110 No. 6, June 2002, Environmental Health Perspectives at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download, indicating 242 pg of TEQ/kg-d at initiation of breastfeeding. Re: EPA’s RfD for dioxin: See reference 6 below.
6) WHO: Air Quality Guidelines, Chapter 5.11 Polychlorinated dibenzodioxins and dibenzofurans, at http://www.euro.who.int/__data/assets/pdf_file/0017/123065/AQG2ndEd_5_11PCDDPCDF.pdf?ua=1
Also UNEP: Results of the global survey on concentrations in human milk of persistent organic pollutants by the United Nations Environment Programme and the World Health Organization, Geneva, 2013, at www.pops.int/TheConvention/ConferenceoftheParties/Meetings/COP6/tabid/3074/cti/Download/mid/9701/Default.aspx?id-85&ObjID=16190 At that page, scroll down about 30 items to the title of this document. See p. 19 in that document.
7) Van den Berg et al., Toxic Equivalency Factors (TEFs) for PCBs, PCDDs, PCDFs for Humans and Wildlife, Environmental Health Perspectives * Volume 106, Number 12, December 1998, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1533232/pdf/envhper00535-0049.pdf
8) Seelbach et al., Polychlorinated Biphenyls Disrupt Blood–Brain Barrier Integrity and Promote Brain Metastasis Formation, Environ Health Perspect, 2010 Apr; 118(4): 479–484. Published online 2009 Oct 28. At https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854723/
9) Baker et al., Adverse effects in adulthood resulting from low-level dioxin exposure in juvenile zebrafish, Endocrine Disruptors, Volume 2, 2014 - Issue 1 Published online: 05 Mar 2014 at https://www.tandfonline.com/doi/full/10.4161/endo.28309
10) ten Tusscher et al., Findings on prenatal, lactational and later childhood exposure to dioxins and dioxin-like compounds: a review of the Amersterdam-Zaandam cohort 1987-2005, AIMS Environmental Science, Volume 2, Issue 1, 1-20, Feb. 2015, at https://www.researchgate.net/publication/272437172_Findings_on_prenatal_lactational_and_later_childhood_exposure_to_dioxins_and_dioxin-like_compounds_a_review_of_the_Amsterdam-Zaandam_cohort_1987-2005
11) CDC: National Vital Statistics Reports: Deaths Final Data for 2015, Nov. 27, 2017, at https://www.cdc.gov/nchs/data/nvsr/nvsr66/nvsr66_06.pdf p. 67
12) CDC: NCHS Data Brief No. 328, Nov. 2018, Mortality in the United States, 2017, at https://www.cdc.gov/nchs/products/databriefs/db328.htm
13) Polychlorinated Biphenyls and Polybrominated Biphenyls, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 107, IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, 2016, Section 1.3.2, and Table 1.14, at
14) Breivik et al., Towards a global historical emission inventory for selected PCB congeners — a mass balance approach: 1. Global production and consumption, Science of Total Environment, Vol. 377, Issues 2-3, May 2007
15) UMassAmherst, Environmental Health and Safety: Polychlorinated Biphenyls (PCBs) - Hazardous Building Materials, at https://ehs.umass.edu/polychlorinated-biphenyls-pcbs-hazardous-building-materials
16) Seltenrich, Incineration Versus Recycling: In Europe, A Debate Over Trash, Yale School of Forestry and Environmental Studies, 2013, at https://e360.yale.edu/features/incineration_versus_recycling__in_europe_a_debate_over_trash
-- Israel Ministry of Environmental Protection: Dangers of Burning Agricultural Waste, at http://www.sviva.gov.il/English/env_topics/AirQuality/Pages/DangersOfBurningWaste.aspx When discussing sources of high concentrations of air pollutants, the Israel Ministry of Environmental Protection states, "The most dangerous emissions can be caused by burning plastics," in large part because of the dioxins produced.
17) EPA: An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000, EPA/600/P-03/002F November 2006, Table 1-12, at https://cfpub.epa.gov/ncea/dioxin/recordisplay.cfm?deid=159286 ; under Downloads, choose to download the Dioxin Inventory of Sources (Optimized Report). See p. xliv and Section 6.5, "Backyard Barrel Burning."
18) Freinkel: A Brief History of Plastic's Conquest of the World, Scientific American, at https://www.scientificamerican.com/article/a-brief-history-of-plastic-world-conquest/
19) ATSDR dioxin document, Toxicological Profile for Chlorinated Dibenzo-p-Dioxins, 1998, pp. 379 and 391, at https://www.atsdr.cdc.gov/toxprofiles/tp104.pdf
20) EPA: Information Sheet 1, Dioxin: Summary of the Dioxin Reassessment Science, 2004 update, at https://semspub.epa.gov/work/06/873707.pdf
21) Winters et al., Trends in dioxin and PCB concentrations in meat samples from several decades of the 20th century, Organohalogen Compd, Vol. 38: 75-78 1998
22) Dioxins and Dioxin-like Compounds in the Food Supply: Strategies to Decrease Exposure, at https://www.ncbi.nlm.nih.gov/books/NBK221718/; go to Chapter 2, A Summary of Dioxin Reports, Assessments, and Regulatory Activity, then go to Dioxin Regulations and Guidelines, then go to "Analytical Methods for Analysis of DLCs in Feeds and Foods" section, then go to Temporal Trends subsection
23) Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment, p 2, http://books.nap.edu/catalog/11688.html, or at https://sph.umich.edu/dioxin/PDF/NRC_HealthRisksfromDioxins.pdf
24) Boekelheide et al., Predicting Later-Life Outcomes of Early-Life Exposures, Environ Health Perspect., Oct 2012, at https://ehp.niehs.nih.gov/cms/attachment/69002320-c37c-4217-ad71-0c7c1d6cf9c2/ehp.1204934.pdf
25) WHO: Don’t pollute my future! The Impact of the Environment on Children’s Health, at http://apps.who.int/iris/bitstream/10665/254678/1/WHO-FWC-IHE-17.01-eng.pdf?ua=1
25a) Barouki et al., Developmental origins of non-communicable disease: Implications for research and public health, Environ Health, 2012, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3384466/
26) Grandjean et al., The Faroes Statement: Human Health Effects of Developmental Exposure to Chemicals in Our Environment, Basic and Clinical Pharmacology and Toxicology, Volume 102, Issue 2, February 2008 at http://onlinelibrary.wiley.com/doi/10.1111/j.1742-7843.2007.00114.x/full
27) ATSDR's Substance Priority List, at https://www.atsdr.cdc.gov/spl/
28) EPA: HEALTH CONSEQUENCES OF DIOXIN EXPOSURE, at https://cfpub.epa.gov/si/si_public_record_Report.cfm?Lab=NHEERL&dirEntryId=171623
29) U.S. ATSDR: Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000, Section 1.6 and Chapter 3, (including Section 3.2.3; in Section 126.96.36.199, “monkeys exposed postnatally to PCB mixtures of congeneric composition and concentration similar to that found in human breast milk showed learning deficits long after exposure had ceased);”also pp. 378 and 423; at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf
30) White and Birnbaum, An Overview of the Effects of Dioxins and Dioxin-like Compounds on Vertebrates, as Documented in Human and Ecological Epidemiology, J Environ Sci Health C Environ Carcinog Ecotoxicol Rev, 2000, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2788749/
31) Seelbach et al., Polychlorinated Biphenyls Disrupt Blood–Brain Barrier Integrity and Promote Brain Metastasis Formation, Environ Health Perspect., 2010 Apr; 118(4): 479–484. Published online 2009 Oct 28. At https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854723/
32) Choi et al., Exercise Attenuates PCB-Induced Changes in the Mouse Gut Microbiome, Environ Health Perspect/; DOI:10.1289/ehp.1306534 at https://ehp.niehs.nih.gov/1306534/
33) Eum et al., Pcbs and Tight Junction Expression, Environ Toxicol Pharmacol, 2009, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2346445/
Selvakumar et al., Polychlorinated biphenyls impair blood-brain barrier integrity via disruption of tight junction proteins in cerebrum, cerebellum and hippocampus of female Wistar rats: neuropotential role of quercetin, Hum Exp. Toxicol., 2013, at https://www.ncbi.nlm.nih.gov/pubmed/23155198
34) CDC: Biomonitoring Summary: Non-Dioxin-Like Polychlorinated Biphenyls, at https://www.cdc.gov/biomonitoring/NDL-PCBs_BiomonitoringSummary.html
35) U.S. ATSDR: Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000, p. 123, at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf
36) Page 372 of ATSDR publication above
37) Texas Spine and Neurosurgery Center web page at https://www.texasspineandneurosurgerycenter.com/pituitary-adenomas/
39) National Academies Press: Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment (2006), Chapter: 6 Noncancer End Points, at https://www.nap.edu/read/11688/chapter/9
40) Jacobson et al., Effects of Exposure to PCBs and Related Compounds on Growth and Activity in Children,
Neurotoxicology and Teratology, 1990, Vol. 12, pp. 319-326, at http://ac.els-cdn.com/089203629090050M/1-s2.0-089203629090050M-main.pdf?_tid=5f238b74-1d4f-11e7-8a29-00000aacb35d&acdnat=1491761419_84450b69c691bfdc5ffd9534957f7940
41) Kostyniak et al., Relation of Lake Ontario Fish Consumption, Lifetime Lactation, and Parity to Breast Milk Polychlorobiphenyl and Pesticide Concentrations, Environmental Research, 1999, at http://www.sciencedirect.com/science/article/pii/S0013935198939391
Great Lakes fish-eaters have been found to have PCB levels about 35% higher than non-fish-eaters for some of the various forms of PCBs; this difference is very small compared with the typical wide variations in people's PCB levels.
41a) Patandin et al., Effects of environmental exposure to polychlorinated biphenyls and dioxins on cognitive abilities in Dutch children at 42 months of age. J Pediatr 134:33–41, 1999.
41b) U.S. ATSDR: Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000, p. 201
42) Two such studies referred to in Chen et al., A 6-Year Follow-Up of Behavior and Activity Disorders in the Taiwan Yu-cheng Children, American Journal of Public Health, Mar. 1994, Vol. 84 No. 3, p. 418 bottom, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1614813/pdf/amjph00454-0081.pdf.
Also Johansen et al., Postnatal exposure to PCB 153 and PCB 180, but not to PCB 52, produces changes in activity level and stimulus control in outbred male Wistar Kyoto rats, Behavioral and Brain Functions, BioMed Central Ltd. 2011, at https://behavioralandbrainfunctions.biomedcentral.com/articles/10.1186/1744-9081-7-18
43) NIH National Cancer Institute: NIH study finds leisure-time physical activity extends life expectancy as much as 4.5 years, Posted: November 6, 2012, at https://www.cancer.gov/news-events/press-releases/2012/PhysicalActivityLifeExpectancy
43a) Abrams et al., Cigarettes: The Rise and Decline, U.S. AHRQ, especially Figure 1, at https://www.ahrq.gov/professionals/education/curriculum-tools/population-health/abrams.html
43b) CDC: HIV and AIDS --- United States, 1981--2000, MMWR June 1, 2001, especially Figure 1, at https://www.cdc.gov/mmwr/preview/mmwrhtml/mm5021a2.htm
43c) White and Birnbaum, An Overview of the Effects of Dioxins and Dioxin-like Compounds on Vertebrates, as Documented in Human and Ecological Epidemiology, J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2009, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2788749/
43d) The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General, at https://www.surgeongeneral.gov/library/reports/50-years-of-progress/fact-sheet.html
44) Lung et al., Incinerator Pollution and Child Development in the Taiwan Birth Cohort Study, Int. J. Environ. Res. Public Health 2013, especially the Supplemental Materials, at www.mdpi.com/1660-4601/10/6/2241/pdf)
45) See www.traffic-pollution-autism.info, Sections B.1 and B.2
46) A 2010 publication of the Oregon Department of Environmental Quality provided information about high exposures of children to PCBs. Oregon Department of Environmental Quality Environmental Cleanup Program, Oct. 2010, 10-LQ-023, p. D2-4 (attachment 2 of Appendix D, near very end) at
www.oregon.gov/deq/FilterDocs/HumanHealthRiskAssessmentGuidance.pdf Regarding dioxins, many studies finding infants to be commonly exposed to high levels of dioxins were carried out in 2000 and later, decades after environmental emissions of dioxins were reported to be declining. (For a summary on this topic, see Section 3 of www.pollutionaction.org/case-deaton-comment.htm)
47) American Academy of Pediatrics: Pediatric Environmental Health, 3rd Edition, 2012, p. 200. "...the relatively high concentration of fat in human milk means that fat-soluble substances will, in effect, concentrate there." Fat-soluble substances that were being discussed included PCBs, PBDEs and various pesticides; dioxins are also fat soluble.
Also Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. Lancet. 2006;368:2167–2178. at https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(06)69665-7/fulltext “Persistent lipophilic substances... such as PCBs, accumulate in maternal adipose tissue and are passed on to the infant in breast milk, resulting in infant exposure that exceeds the mother’s own exposure by 100-fold on the basis of bodyweight.”
Also ATSDR: Toxicological Profile for Polychlorinated Biphenyls (PCBs) at https://www.atsdr.cdc.gov/toxprofiles/tp17.pdf
p. 393: "The daily TEQ intake per kg body weight is about 50 times higher in breast-fed infants and 3 times higher in toddlers than in adults."
Also see Section 2.b at www.pollution-effects.info/
48) Mocarelli et al., Perinatal Exposure to Low Doses of Dioxin Can Permanently Impair Human Semen Quality, Environ Health Perspect. May 2011; 119(5): 713–718. Published online Jan 24, 2011 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3094426/
48a) Quinn et al., Investigating Intergenerational Differences in Human PCB Exposure due to Variable Emissions and Reproductive Behaviors, Environ Health Perspect. May 2011; 119(5): 641–646. at www.ncbi.nlm.nih.gov/pmc/articles/PMC3094414
--Jacobson et al., Determinants of polychlorinated biphenyls (PCBs), polybrominated biphenyls (PBBs), and dichlorodiphenyl trichloroethane (DDT) levels in the sera of young children, Am J Public Health. 1989 October; 79(10): 1401–1404
-- Table 1 in Jusko et al., Prenatal and Postnatal Serum PCB Concentrations and Cochlear Function in Children at 45 Months of Age, Environmental Health Perspectives, 22 July 2014 (Advance Pub.) at http://ehp.niehs.nih.gov/wp-content/uploads/advpub/2014/7/ehp.1307473.pdf
-- Danish Health and Medicines Authority, Health risks of PCB in the indoor climate in Denmark, 2013, at http://sundhedsstyrelsen.dk/~/media/D290AF38C2114775804F1B6BDD6841C6.ashx
-- Ayotte et al., Assessment of Pre- and Postnatal Exposure to Polychlorinated Biphenyls:
Lessons from the Inuit Cohort Study, Environmental Health Perspectives • Volume 111 | Number 9 | July 2003, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241583/pdf/ehp0111-001253.pdf (finding 6.6-fold increase in infant PCB levels with over three months of breastfeeding, compared with no breastfeeding -- see Table 4)
-- Trnovec et al., Assessment of exposure to PCB 153 from breast feeding and normal food intake in individual children using a system approach model, Chemosphere, Dec. 2011, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228605/
49) Kerger et al., An Adaptable Internal Dose Model for Risk Assessment of Dietary and Soil Dioxin Exposures in Young Children, Toxicological Sciences 100(1), 224–237 (2007), at https://academic.oup.com/toxsci/article/100/1/224/1623981
Lorber et al., Infant Exposure to Dioxin-like Compounds in Breast Milk, Vol. 110 No. 6, June 2002, Environmental Health Perspectives at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download,
50) USDA: Dioxins in the Food Chain: Background, at https://www.aphis.usda.gov/animal_health/emergingissues/downloads/dioxins.pdf
EPA: Information Sheet 1: Dioxin: Summary of the Dioxin Reassessment Science, 2004 update, USDA: Dioxins in the Food Chain: Background, at https://www.aphis.usda.gov/animal_health/emergingissues/downloads/dioxins.pdf
Roveda et al., [Exposure to polychlorinated biphenyls (PCBs) in food and cancer risk: recent advances], lg Sanita Pubbl., 2006, at https://www.ncbi.nlm.nih.gov/pubmed/17256022
51) Lorber et al., Infant Exposure to Dioxin-like Compounds in Breast Milk, Vol. 110 No. 6, June 2002, Environmental Health Perspectives, Figure 3, at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download,
52) Mocarelli et al., Perinatal Exposure to Low Doses of Dioxin Can Permanently Impair Human Semen Quality, Environ Health Perspect. May 2011; 119(5): 713–718. Published online Jan 24, 2011. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3094426/
53) Greiner, Exclusive breastfeeding: measurement and indicators, Int Breastfeed J., 2014, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4209171/
53a) SJ Fomon, Infant feeding in the 20th Century: Formula and Beikost, J Nutr, Feb. 2001, Fig. 5, at http://jn.nutrition.org/content/131/2/409S.full
53b) Riordan and Countryman, Basics of breastfeeding. Part I: Infant feeding patterns past and present, JOGN Nurs, 1980, at https://www.ncbi.nlm.nih.gov/pubmed/7001126
53c) American Academy of Family Physicians, Breastfeeding, Family Physicians Supporting (Position Paper), at https://www.aafp.org/about/policies/all/breastfeeding-support.html
53d) Nutrition During Lactation: 3. Who Breastfeeds in the United States? Institute of Medicine (US) Committee on Nutritional Status During Pregnancy and Lactation, National Academies Press, 1991, at https://www.ncbi.nlm.nih.gov/books/NBK235588/
53e) Livingston, No Bottles, No Pacies’ and No Cupcakes: A Feminist Analysis of Motherhood in La Leche League, M.A. thesis at Univ. of North Carolina at Chapel Hill, p. 15, referring to first edition of The Womanly Art of Breastfeeding, at https://cdr.lib.unc.edu/indexablecontent/uuid:cc140b45-ceca-4729-a1f4-49d12f091664
54) UNICEF: 1990-2005: Celebrating the Innocenti Declaration on the Protection, Promotion and Support of Breastfeeding, pp. 11, 12, at https://www.ennonline.net/attachments/27/innocenti-declaration-1990-2005-book.pdf
55) WHO: Baby-friendly Hospital Initiative, at https://www.who.int/nutrition/topics/bfhi/en/
56) Greiner, Exclusive breastfeeding: measurement and indicators, Int Breastfeed J., 2014, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4209171/
CDC: MMWR Weekly, Aug. 3, 2007: Breastfeeding Trends and Updated National Health Objectives for Exclusive Breastfeeding --- United States, Birth Years 2000--2004, at https://www.cdc.gov/mmwr/preview/mmwrhtml/mm5630a2.htm
57) Wright et al., Changing Hospital Practices to Increase the Duration of Breastfeeding, Pediatrics, Vol. 97 No. 5 May 1996
58) CDC, Kochanek et al., Mortality in the United States, 2016 (Data table for Figure 3), NCHS Data Brief No. 293 December 2017, at https://www.cdc.gov/nchs/data/databriefs/db293.pdf ;
59) AAP Committee on Nutrition: Pediatric Nutrition Handbook, Third Edition, 1993 (preface dated Nov., 1992),
CDC (Sherry et al.): Mortality in the United States, 2017, NCHS Data Brief, No. 328 November 2018, at https://www.cdc.gov/nchs/data/databriefs/db328-h.pdf
60) Breastfeeding and the Use of Human Milk, Work Group on Breastfeeding, Pediatrics, Dec. 1997, at http://pediatrics.aappublications.org/content/100/6/1035
61) CDC, Kochanek et al., Mortality in the United States, 2016 (Data table for Figure 3), NCHS Data Brief No. 293 December 2017, at https://www.cdc.gov/nchs/data/databriefs/db293.pdf ;
CDC (Sherry et al.): Mortality in the United States, 2017, NCHS Data Brief, No. 328 November 2018, at https://www.cdc.gov/nchs/data/databriefs/db328-h.pdf
62) Howard, Minimum Latency & Types or Categories of Cancer, World Trade Center Health Program November 7, 2014, at https://www.cdc.gov/wtc/pdfs/policies/wtchpminlatcancer2014-11-07-508.pdf
63) CDC: U.S. breastfeeding rates continue to rise, at https://www.cdc.gov/media/releases/2013/p0731-breastfeeding-rates.html and CDC: Breastfeeding Report Card 2018 at https://www.cdc.gov/breastfeeding/data/reportcard.htm
64) The author of this article sent letters of inquiry to the American Academy of Pediatrics, the American Academy of Family Physicians, and the entire science team at the major autism-advocacy organization, Autism Speaks. Those letters asked whether the addressees or their organizations were aware of (a) any toxins that are believed to widely reach infants in doses well in excess of a recognized safe level (e.g., EPA’s RfD), aside from the several such toxins that are ingested by means of breast milk, or (b) any other pathway of infant exposure to toxins in concentrations exceeding established safe levels. As of six or more months later, none of the four replies that were received suggested any other such toxins or other pathway.
65) CDC: Suicide Facts at a Glance, at https://www.cdc.gov/violenceprevention/pdf/suicide-datasheet-a.pdf
66) Texas Spine and Neurosurgery Center web page at https://www.texasspineandneurosurgerycenter.com/pituitary-adenomas/
67a) WHO: State of the Science: Endocrine Disrupting Chemicals - 2012, p. 119 State of the Science of Endocrine Disrupting Chemicals - 2012, accessible at https://www.who.int/ceh/publications/endocrine/en/
68) Remafedi et al., The Relationship between Suicide Risk and Sexual Orientation: Results of a Population-Based Study, American Journal of Public Health, 1998, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1508407/pdf/amjph00013-0059.pdf
69) Feinleib, Report of the Secretary's Task Force on Youth Suicide. Volume 3: Prevention and Interventions in Youth Suicide, p. 3-10, DHHS. Alcohol, Drug Abuse, and Mental Health Administration Jan 89
69a) Harvard Institute of Economic Research: Explaining the Rise in Youth Suicide, 2001, Harvard University, at https://canadiancrc.com/pdfs/harvard_discussion_paper_no_1917.pdf
69b) Harvard Institute of Economic Research: Explaining the Rise in Youth Suicide, 2001, Harvard University, at https://canadiancrc.com/pdfs/harvard_discussion_paper_no_1917.pdf p. 32
69c) "Doubtful treatment" in Advancing Suicide Prevention, July/August 2005, Vol. 1, Issue 2, p. 13, Science Matters, at www.advancingsp.org/ASP_July_August_2005.pdf
69d) CDC National Biomonitoring Program: Dioxin-Like Chemicals: Polychlorinated Dibenzo-p-dioxins, Polychlorinated Dibenzofurans, and Coplanar and Mono-ortho-substituted Polychlorinated Biphenyls, at https://www.cdc.gov/biomonitoring/DioxinLikeChemicals_BiomonitoringSummary.html
69e) GW Chance, Environmental contaminants and children’s health: Cause for concern, time for action, Paediatr Child Health. 2001 Dec; 6(10): 731–743. at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805986/
69f) Simon and Herkes, The neurologic manifestations of the acute porphyrias, J Clin Neurosci, 2011, at https://www.ncbi.nlm.nih.gov/pubmed/21724399
69g) Crimlisk, The little imitator-porphyria: a neuropsychiatric disorder, Journal of Neurology, Neurosurgery and Psychiatry, 1997,at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1074085/pdf/jnnpsyc00004-0015.pdf
69h) Mayo Clinic: Peripheral neuropathy, at https://www.mayoclinic.org/diseases-conditions/peripheral-neuropathy/symptoms-causes/syc-20352061
69k) Mayo Clinic: Porphyria at https://www.mayoclinic.org/diseases-conditions/porphyria/symptoms-causes/syc-20356066
69m) Youth suicide rate in rural areas is nearly double the rate in cities, Science Daily, Mar. 9, 2015, citing Ohio State Univ. source, at https://www.sciencedaily.com/releases/2015/03/150309123954.htm
69n) Nielssen et al., High rates of suicide attempt in early-onset psychosis are associated with depression, anxiety and previous self-harm, BMJ Journals, 2014, at https://ebmh.bmj.com/content/17/4/101
69o) Kauppinen et al., Prognosis of acute porphyria: occurrence of acute attacks, precipitating factors, and associated diseases, Medicine (Baltimore), 1992, at https://www.ncbi.nlm.nih.gov/pubmed/1549056
69p) O'Malley et al., Porphyria: often discussed but too often missed, Pract Neurol., 2018, at https://www.ncbi.nlm.nih.gov/pubmed/29540448
69q) Colt: November of the Soul: The Enigma of Suicide, Simon and Schuster, 1991. p. 248
69r) Singh and Siahpush, Increasing Rural–Urban Gradients in US Suicide Mortality, 1970–1997, Am J Public Health, 2002, Figure 1, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1447208/ The study's data (in Figure 1) shows suicide rates to still be higher in urban than in rural areas as of 1970, but suicides were increasing in rural areas and declining in urban areas at that time; by the early 1980's, suicide rates in rural areas were starting to become higher than in urban areas, and the difference widened in subsequent years
69s) Scientific statement on the health-based guidance values for dioxins and dioxin-like PCBs, European Food Safety Authority, EFSA Journal, 2015, at https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/j.efsa.2015.4124
-- Also European Food Safety Authority Panel on Contaminants in the Food Chain (CONTAM), Risk for animal and human health related to the presence of dioxins and dioxin-like PCBs in feed and food, Nov. 2018, at https://efsa.onlinelibrary.wiley.com/doi/10.2903/j.efsa.2018.5333
69t) European Food Safety Authority: Dioxins and related PCBs: tolerable intake level updated, Nov. 2018, at https://www.efsa.europa.eu/en/press/news/181120
69u) EPA: An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000; especially see Table 1-12 (Note quantities for year 2000 and see MINIMALLY CONTROLLED OR UNCONTROLLED COMBUSTIONf 2-3 pages into that Table); at ofmpub.epa.gov/eims/eimscomm.getfile?p_download_id=523391
70) Fomon: Infant feeding in the 20th Century: Formula and Beikost, J. Nutr., Feb. 2001, Fig. 5, at http://jn.nutrition.org/content/131/2/409S.full
71) AAP Policy Statement on breastfeeding, at http://pediatrics.aappublications.org/content/129/3/e827.full#content-block
72) Martin et al., Effects of Promoting Long-term, Exclusive Breastfeeding on Adolescent Adiposity, Blood Pressure, and Growth Trajectories: A Secondary Analysis of a Randomized Clinical Trial, JAMA Pediatrics, at https://jamanetwork.com/journals/jamapediatrics/fullarticle/2624341
73) O'Neil and 7 others, Observational evidence and strength of evidence domains: case examples, Biomed Central: Systematic Reviews, at https://systematicreviewsjournal.biomedcentral.com/articles/10.1186/2046-4053-3-35
Gary Taubes, Do We Really Know What Makes Us Healthy? The New York Times Magazine, Sept. 16, 2007, at http://www.nytimes.com/2007/09/16/magazine/16epidemiology-t.html?_r=0
Also see references in letter to AAP
Also see reference 73b just below.
73b) See Section 10 of www.pollution-effects.info
74) Type 2 Diabetes in Children and Young Adults: A “New Epidemic” Francine Ratner Kaufman, MD CLINICAL DIABETES • Volume 20, Number 4, 2002 at http://clinical.diabetesjournals.org/content/20/4/217.full.pdf+html
Also, a Univ. of Michigan article published in 2008 reported, “Recent studies suggest that there have been dramatic increases in type 2 diabetes among individuals in their 20s and 30s...." (at http://www2.med.umich.edu/prmc/media/newsroom/details.cfm?ID=422), which is compatible with origins of the epidemic in infant development after 1972.
76) CDC: U.S. breastfeeding rates continue to rise, at https://www.cdc.gov/media/releases/2013/p0731-breastfeeding-rates.html and CDC: Breastfeeding Report Card 2018 at https://www.cdc.gov/breastfeeding/data/reportcard.htm
77) Houtrow et al., Changing Trends of Childhood Disability, 2001–2011, Pediatrics Vol. 134 No. 3 September 1, 2014, especially Table 3, at http://pediatrics.aappublications.org/content/134/3/530.abstract , Table 2
77a) The Surgeon General’s Call to Action to Support Breastfeeding 2011, Table 2, at www.surgeongeneral.gov/library/calls/breastfeeding/calltoactiontosupportbreastfeeding.pdf
77b) CDC: IFPS2 - Chapter 3, Table 3.4, (Infant Feeding Practices Study II; Survey carried out 2006-2007) at https://www.cdc.gov/breastfeeding/pdf/ifps/data/ifps2_tables_ch3.pdf. This table shows exclusive breastfeeding rates as of 2007-2007, which indicate growth since the early 1990's, since exclusive breastfeeding was authoritatively considered to be almost zero in the early 1990's.56
77c) Rates of Any and Exclusive Breastfeeding by Socio-demographics among Children Born in 2009 (based on dual-frame (landline and cellular telephone) samples from 2011 and 2012 National Immunization Surveys) at https://www.cdc.gov/breastfeeding/data/nis_data/rates-any-exclusive-bf-socio-dem-2009.htm. This table shows exclusive breastfeeding rates as of 2011-2012, which indicate growth since the early 1990's, since exclusive breastfeeding was authoritatively considered to be almost zero in the early 1990's.56
78) Pastor et al., Diagnosed attention deficit hyperactivity disorder and learning disability: United States 2004-2006, National Center for Health Statistics, 2008, at http://www.cdc.gov/nchs/data/series/sr_10/Sr10_237.pdf
79) Barouki et al., Developmental origins of non-communicable disease: Implications for research and public health, Environ Health. 2012; 11: 42. PMCID: PMC3384466 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3384466/
79a) "Ready, Willing, and Unable to Serve," Mission: Readiness, 2009, signed by over 70 retired U.S. generals and admirals, at http://cdn.missionreadiness.org/NATEE1109.pdf
79b) NLTS and NLTS Wave 1 parent interviews and federal child count statistics (U.S. Department of Education, 1989 and Office of Special Education Programs, 2002), Exhibit 2-1, at http://nlts2.org/reports/2003_04-1/nlts2_report_2003_04-1_complete.pdf
80) Monthly Labor Review, Nov. 1993, p. 7, at http://www.bls.gov/mlr/1993/11/art1full.pdf of U.S. Bureau of Labor Statistics website.
81) CDC: NCHS - Death rates and life expectancy at birth, at https://data.cdc.gov/NCHS/NCHS-Death-rates-and-life-expectancy-at-birth/w9j2-ggv5
82) On average, people born in the U.S. in 2015 will live 36.5 days fewer than those born in 2014, LA Times, Dec. 08, 2016, at https://www.latimes.com/science/sciencenow/la-sci-sn-us-life-expectancy-drops-20161208-story.html
83) University of California at San Francisco: Breastfeeding, Brain Development and Chemical Poisons: Neuroscientist Michael Merzenich, By Jeff Miller, May 18, 2007 at https://www.ucsf.edu/news/2007/05/3817/merzenich . Re Dr. Merzenich: see http://www.brainhq.com/world-class-science/science-team/dr-michael-merzenich.
84) EPA: Technical Fact Sheet on PBDEs, at https://www.epa.gov/sites/production/files/2014-03/documents/ffrrofactsheet_contaminant_perchlorate_january2014_final_0.pdf
85) Kenet et al., Perinatal exposure to a noncoplanar polychlorinated biphenyl alters tonotopy, receptive fields, and plasticity in rat primary auditory cortex, 2007, The National Academy of Sciences of the USA, 7646–7651, PNAS, May 1, 2007, vol. 104, no. 18, at http://www.pnas.org/content/104/18/7646.full.pdf
86) Merzenich, What underlies the documented increase in autism incidence? Results of a new study,
from On the Brain, by Dr. Michael Merzenich, 26 April 2007, at http://www.onthebrain.com/2007/04/underlies-documented-increase-autism-incidence-results-new-study
Also: Breastfeeding, Brain Development and Chemical Poisons: Neuroscientist Michael Merzenich, by Jeff Miller on May 18, 2007, at https://www.ucsf.edu/news/2007/05/3817/merzenich: "...the levels of PCBs to which the laboratory rats were exposed proportionately equal the levels now being found in the breast milk of women all over the country."
87) WHO, Persistent Organic Pollutants: Impact on Child Health, p. 6, at http://whqlibdoc.who.int/publications/2010/9789241501101_eng.pdf
88) Collaborative on Health and the Environment’s Learning and Developmental Disabilities Initiative: Scientific Consensus Statement on Environmental Agents Associated with Neurodevelopmental Disorders, 2008, at https://www.healthandenvironment.org/docs/xaruploads/LDDIStatement.pdf
89) Stein et al., In Harm’s Way: Toxic Threats to Child Development, Journal of Developmental & Behavioral Pediatrics: February 2002 - Volume 23 - Issue 0 - pp S13-S22 at http://journals.lww.com/jrnldbp/Fulltext/2002/02001/In_Harm_s_Way__Toxic_Threats_to_Child_Development.4.aspx
90) Giordano et al., Developmental Neurotoxicity: Some Old and New Issues, ISRN Toxicol. 2012; 2012: 814795, PMCID: PMC3658697 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658697
90a) Brominated Flame Retardants, Third annual report to the Maine Legislature, Jan. 2007, Maine Dept. of Environmental Protection, Maine Center for Disease Control and Prevention, Dr. Deborah Rice et al., at http://www.maine.gov/dep/waste/publications/legislativereports/documents/finalrptjan07.pdf
91) EPA Polybrominated Diphenyl Ethers Action Plan at http://www.epa.gov/sites/production/files/2015-09/documents/pbdes_ap_2009_1230_final.pdf, p. 12. Quoting from p. 12: "PBDEs are a concern for children’s health. The most sensitive outcome of PBDE exposure is adverse neurobehavioral effects following exposure during the postnatal period."
92) Gascon M. et al., Effects of pre and postnatal exposure to low levels of polybromodiphenyl ethers on neurodevelopment and thyroid hormone levels at 4 years of age Environ Int. 2011 Apr;37(3):605-11. doi: 10.1016/j.envint.2010.12.005. Epub 2011 Jan 14 found at www.ncbi.nlm.nih.gov/pubmed/21237513
93) Gascon et al., Polybrominated Diphenyl Ethers (PBDEs) in Breast Milk and Neuropsychological Development in Infants US National Library of Medicine National Institutes of Health Environ Health Perspect v.120(12); Dec 2012 > PMC3548276 Environ Health Perspect. 2012 December; 120(12): 1760–1765. at www.ncbi.nlm.nih.gov/pmc/articles/PMC3548276
94) Chao et al., Levels of Breast Milk PBDEs From Southern Taiwan and Their Potential Impact on Neurodevelopment, Pediatric Research (2011) 70, 596–600; doi:10.1203/PDR.0b013e3182320b9b at http://www.nature.com/pr/journal/v70/n6/pdf/pr20111086a.pdf?origin=publication_detail
95) Martin et al., A Human Mixture Risk Assessment for Neurodevelopmental Toxicity Associated with Polybrominated Diphenyl Ethers Used as Flame Retardants, Environ Health Perspect, 2017 Aug at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5783671/;
Hazard Index based on reference doses from EFSA (European Food Safety Authority). 2011. EFSA Panel on Contaminants in the Food Chain (CONTAM); Scientific Opinion on Polybrominated Diphenyl Ethers (PBDEs) in Food. EFSA J 9(5):2156
96) Trasande et al., Burden of disease and costs of exposure to endocrine disrupting chemicals in the European Union: an updated analysis, Andrology, 2016 Jul, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5244983/
97) Giordano et al., Developmental Neurotoxicity: Some Old and New Issues, ISRN Toxicol. 2012; 2012: 814795, PMCID: PMC3658697 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658697
98) In the first study described, the comparisons were made between children with detectable levels of PBDEs versus those without detectable levels; in the second one, the basic comparisons were made among three different groups according to levels of exposure, with the most-exposed group being made up of over 40% of the population; comparisons were made between those in which the PBDE level was quantifiable, those in which it was undetectable, and those in which it was detectable but not quantifiable.(Table 2 of Gascon et al. 2012)
99) Schecter et al., Polybrominated Diphenyl Ether (PBDE) Levels in an Expanded Market Basket Survey of U.S. Food and Estimated PBDE Dietary Intake by Age and Sex, Environ Health Perspect. 2006 Oct; 114(10): 1515–1520.Published online 2006 Jul 13. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1626425
100) Eskenazi et al. 2013. In Utero and Childhood Polybrominated Diphenyl Ether (PBDE) Exposures and Neurodevelopment in the CHAMACOS Study. Environmental Health Perspectives 121(2):257-262, including.Supplemental Materials Table S5, at
102) Costa and Giordano, Developmental Neurotoxicity Of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, 2008 Neurotoxicology National Center for Biotechnology Information, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052
103) 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, 2001, edited by Charles A. Nelson and Monica Luciana. Selected pages can be found at no charge at http://www.worldcat.org/title/handbook-of-developmental-cognitive-neuroscience/oclc/45059115/viewport.
Also Stephen B. Klein and B. Michael Thorne in Biological Psychology (2006), Worth Publishers, p. 390
104) EPA: Technical Fact Sheet on PBDEs, at https://www.epa.gov/sites/production/files/2014-03/documents/ffrrofactsheet_contaminant_perchlorate_january2014_final_0.pdf
105) Shamberger, R.J., Autism rates associated with nutrition and the WIC program, J Am Coll Nutr. 2011 Oct;30(5):348-53. Abstract at www.ncbi.nlm.nih.gov/pubmed/22081621
106) Dodds et al., The Role of Prenatal, Obstetric and Neonatal Factors in the Development of Autism, J Autism Dev Disord (July 2011) 41:891–902 DOI 10.1007/s10803-010-1114-8, Table 6, at
107) Breastfeeding and Autism P. G. Williams, MD, Pediatrics, University of Louisville, and L. L. Sears, PhD, presented at International Meeting for Autism Research, May 22, 2010, Philadelphia Marriot https://imfar.confex.com/imfr/2010/webprogram/Paper6362.html) This study found a 37% rate of breastfeeding at six months among children diagnosed with autism, as compared with 13% in the control group.
108) P. 253 of Sullivan, Temporality of Risk Factors and the Gender Differential Related to Autism Spectrum Disorder Diagnosis (PhD thesis), Walden University Scholar Works, 2015, at http://scholarworks.waldenu.edu/cgi/viewcontent.cgi?article=1274&context=dissertations
109) Lynch et al., The effect of prenatal and postnatal exposure to polychlorinated biphenyls and child neurodevelopment at age twenty four months, Reprod Toxicol. 2012 Nov;34(3):451-6. doi: 10.1016/j.reprotox.2012.04.013. Epub 2012 May 5. at http://www.sciencedirect.com/science/article/pii/S0890623812000755
110) Husk et al., Breastfeeding and Autism Spectrum Disorder in the National Survey of Children's Health, Epidemiology. 2015 Jul;26(4):451-7. Table 3 and accompanying text, and p. 454, bottom left. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/25872161
111) See Section 4.a.2.a at http://www.pollution-effects.info for published sources of this information.
112) CDC: Opioid Overdose: Understanding the Epidemic at https://www.cdc.gov/drugoverdose/epidemic/index.html
113) CDC: CDC's Response to the Opioid Overdose Epidemic, at https://www.cdc.gov/opioids/strategy.html
114) Chen et al., Prevention of Prescription Opioid Misuse and Projected Overdose Deaths in the United States, JAMA Network Open, Feb.1, 2019, at https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2723405
115) Institute of Medicine of the National Academies: Relieving Pain in America: A Blueprint, 2011, pp. 55, 62, 63 at https://www.nap.edu/download/13172
116) White and Birnbaum, An Overview of the Effects of Dioxins and Dioxin-like Compounds on Vertebrates, as Documented in Human and Ecological Epidemiology, J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2009 Oct; 27(4): 197–211, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2788749/
ALSO Carpenter, Ed.: Effects of Persistent and Bioactive Organic Pollutants on Human Health, Wiley, 2013, section on Dioxin-like Chemicals
117) .Riihimäki, Low-back pain, its origin and risk indicators, Scandinavian Journal of Work, Environment & Health, Vol. 17, No. 2 (April 1991), pp. 81-90, at http://www.jstor.org/stable/40965865
118) ,Lee et al., PCB126 induces apoptosis of chondrocytes via ROS-dependent pathways, Osteoarthritis and Cartilage, Vol. 20, 2012, at https://www.sciencedirect.com/science/article/pii/S1063458412008588
Also Abella et al., Environmental pollutants and osteoarthritis: Effects of non-dioxin-like polychlorinated biphenyls on cultured chondrocytes, Osteoarthritis and Cartilage Vol. 22, Supplement, Apr 2014, at https://www.sciencedirect.com/science/article/pii/S1063458414003653
119) NIH: Low Back Pain Fact Sheet, at https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Low-Back-Pain-Fact-Sheet;
Also UK – National Health Service: Exercises for sciatica, at https://www.nhs.uk/live-well/exercise/exercises-for-sciatica/
120) The National Academy of Sciences: Pain Management and the Opioid Epidemic (2017), p. 189, National Academies Press, at https://www.nap.edu/read/24781/chapter/8#189
121) deShazo et al., Backstories on the US Opioid Epidemic. Good Intentions Gone Bad, an Industry Gone Rogue, and Watch Dogs Gone to Sleep, American Journal of Medicine, June 2018, at https://www.amjmed.com/article/S0002-9343(18)30084-6/fulltext
122) bar graph in S. Okie, A Flood of Opioids, a Rising Tide of Deaths, New England Journal of Medicine, Nov. 18, 2010, at https://www.nejm.org/doi/full/10.1056/nejmp1011512
123) Phillips DM. JCAHO pain management standards are unveiled. Joint Commission on Accreditation of Healthcare Organizations. JAMA 2000; 284:428-429.
124) CDC: NCIPC Board of Scientific Counselors, Jan 28, 2016, at https://www.cdc.gov/maso/facm/pdfs/BSCNCIPC/20160128_ncipcbsc.pdf, pp. 12, 20, 24, 39, 50, Appendix B
125) Pain Management and the Intersection of Pain and Opioid Use Disorder, Ch. 2, p. 86, National Academies Press, 2017, at https://www.nap.edu/read/24781/chapter/5#86
126) Pain Management and the Intersection of Pain and Opioid Use Disorder, Ch. 2, p. 86, National Academies Press, 2017, at https://www.nap.edu/read/24781/chapter/5#86
127) Research on the Use and Misuse of Fentanyl and Other Synthetic Opioids,June 30, 2017, presented by Wilson M. Compton, M.D., Deputy Director, House Committee on Energy and Commerce, Subcommittee on Oversight and Investigations, at https://www.drugabuse.gov/about-nida/legislative-activities/testimony-to-congress/2017/research-use-misuse-fentanyl-other-synthetic-opioids
128) Cunha-Oliveira et al., Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs, Brain Research Reviews 58 (2008)
129) Facing Addiction in America: The Surgeon General's Report on Alcohol, Drugs, and Health [Internet]. CHAPTER 2THE NEUROBIOLOGY OF SUBSTANCE USE, MISUSE, AND ADDICTION, at https://www.ncbi.nlm.nih.gov/books/NBK424849/
Also Surgeon General’s Report on Alcohol, Drugs, and Health: The Neurobiology of Substance Use, Misuse, and Addiction, at https://addiction.surgeongeneral.gov/index.php/executive-summary/report/neurobiology-substance-use-misuse-and-addiction
130) Girault and Greengard, The Neurobiology of Dopamine Signaling, Arch Neurol. 2004;61(5): JAMA Neurology, at https://jamanetwork.com/journals/jamaneurology/fullarticle/785704
131) Dip in dopamine linked with drug addiction, in News, of MRC London Institute of Medical Sciences, London, 17 March 2017, at https://lms.mrc.ac.uk/dip-dopamine-linked-drug-addiction/
Also see ref #132 below
132) NIH National Institute on Drug Abuse: Social Environment Appears Linked to Biological Changes in Dopamine System, May Influence Vulnerability to Cocaine Addiction, accessed March, 2019, at https://archives.drugabuse.gov/news-events/nida-notes/2003/01/social-environment-appears-linked-to-biological-changes-in-dopamine-system-may-influence
133) Substance Abuse and Mental Health Services Administration (US): Treatment for Stimulant Use Disorders: Chapter 2—How Stimulants Affect the Brain and Behavior, 1999, at https://www.ncbi.nlm.nih.gov/books/NBK64328/
Also Olgjuin et al.,The Role of Dopamine and Its Dysfunction as a Consequence of Oxidative Stress, Oxidative Medicine and Cellular Longevity, Volume 2016, Article ID 9730467, at https://www.hindawi.com/journals/omcl/2016/9730467/
134) Dopamine Deficiency: 8 Ways to Naturally Overcome Depression, University Health News Daily, at https://universityhealthnews.com/daily/depression/8-natural-dopamine-boosters-to-overcome-depression/
135) Okie, A Flood of Opioids, a Rising Tide of Deaths, New England Journal of Medicine, Nov. 18, 2010, at https://www.nejm.org/doi/full/10.1056/nejmp1011512
136) CDC: Data Overview: Overdose deaths from opioids, including prescription opioids, heroin, and synthetic opioids (like fentanyl) have increased almost six times since 1999, at https://www.cdc.gov/drugoverdose/data/index.html
There is almost certainly no other source of harm
-- to which many Americans have been exposed with such rapid increases and
-- which has been found to affect widely-distributed people in concentrations that far exceed established safe levels (Section 4.c) and
-- recognized effects of which are compatible with typical characteristics of people of concern, in likelihood of chronic pain, of being drawn to addictive substances, ethnicity……….,
the vast majority of those who started their abuse (of heroin) after 1990, did so with prescription opioids. Cicero et al., The Changing Face of Heroin Use in the United States, JAMA Psychiatry, 2014
Most contemporary opioid misuse started with prescription opioids. <<Research on the Use and Misuse of Fentanyl and Other Synthetic Opioids,June 30, 2017, presented by Wilson M. Compton, M.D., Deputy Director, House Committee on Energy and Commerce, Subcommittee on Oversight and Investigations, at https://www.drugabuse.gov/about-nida/legislative-activities/testimony-to-congress/2017/research-use-misuse-fentanyl-other-synthetic-opioids
Headaches the other of the two most common sources of chronic pain. And the prevalence of chronic pain increases with age. <Tompkins et al.,Providing chronic pain management in the “Fifth Vital Sign” Era: Historical and treatment perspectives on a modern-day medical dilemma, Drug Alcohol Depend, 2017 Apr, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5771233/)
PCBs and dioxins are also implicated as causes of sciatica (lower back pain), one of the two leading causes of chronic pain. (See Section 9 of the Pollution Action website at http://www.pollutionaction.org/case-deaton-comment.htm#sec9);