Toxins in Breast Milk and those in Formula or Cow's Milk
The pro-breastfeeding organization, MOMS (Making Our Milk Safe) lists various chemicals found in human breast milk, including Bisphenol A (BPA -- endocrine disruptors, which are toxic to infant development), perchlorate (used in rocket fuel), perfluorinated chemicals (PFCs, used in floor cleaners and non-stick pans), polyvinyl chloride (PVC, commonly known as vinyl) and the heavy metals cadmium, lead and mercury.(1) According to a 2015 statement by the International Federation of Gynecology and Obstetrics, “Exposure to toxic chemicals during pregnancy and lactation is ubiquitous. Research based on representative sampling of the population at large has documented that virtually every pregnant woman in the USA has at least 43 different environmental chemicals in her body.”(1a) Researchers have identified 200 different chemical contaminants in the milk of U.S. mothers.(2) That figure was as of a study published in 1982, and many new chemicals have been added to the environment since then.
Experts on the subject of toxins in breast milk pointed out in 2004 that "these substances have caused contamination of human milk only during the last half century, and long-term health impacts are now being discovered."(3) The International Federation of Gynecology and Obstetrics, quoted above, apparently sees effects of the toxins that are currently being transferred during pregnancy and lactation, stating that “Rates of non-communicable diseases (NCDs) such as cancer, cardiovascular disease, chronic respiratory disease, and diabetes are increasing, and the high rate of NCDs seen in high-income countries is now also emerging as a health crisis among middle- and low-income countries [51,52]…." Continuing, "These trends have occurred in a timeframe inconsistent with a much slower pace of changes in the human genome, indicating that the environment (meaning environmental toxins) has shaped these disease patterns.” (emphasis and parenthetical expression added)
So conventional wisdom about breastfeeding that was well suited to the realities of earlier times may have little relevance in typical contemporary environments in developed countries.
The EPA has determined that the reasonably-safe upper threshold of daily exposure to the neuro-developmental toxin and carcinogen, dioxin, is 0.7 pg TEQ/kg-day (toxic equivalency per kilogram of body weight per day).(4) The body-weight-based dose received by an apparently typical breastfeeding U.S. infant at initiation of nursing was found to be more than 300 times that estimated safe exposure, at 242 pg TEQ.(5) Confirmation of that range of exposure (bearing in mind the known decline in the dioxin dose in breast milk as the woman’s stored concentrations are excreted in her milk) is indicated by a figure quoted in a British Medical Journal publication of 170 pg at two months after birth; other UK data showed a mean of 41 pg at 5-6 months, but they referred to a Dutch study that found levels two to five times as high.(6) The other readily-found studies of this infant exposure, conducted in Germany, Korea, Netherlands, Czech Republic, France, Greece, Japan, China, and Slovakia, and all published in the 2000's, arrived at similar figures; the major upward deviation was in Japan, where a large part of the figures were even higher than the general range.(7) In Poland, the exposure was lower than the general range, but still 17 times higher in breast milk than in infant formula.(7a)
Known exposures of breastfed infants to mercury are several times higher than the maximum level allowed by U.S. law in bottled water. (see Section 1.c below) Exposure of breastfed infants to PBDEs, which have been increasing in human milk especially rapidly in recent decades, are also far above the EPA’s established safe level. (see Section 1.c below) PCBs are present in human milk at about 20 times the level allowed in public water supplies in the U.S.(12c) Perchlorate, another strongly-suspected neuro-developmental toxin, has been found in breast milk in concentrations greatly exceeding the limit for that chemical set by the state of California (see Section 1.g below).
These unsafe exposures of breastfed infants come at the most vulnerable times of the children's lives for neurological development, and they come shortly before a high-level period for development of childhood cancer. (see www.breastfeeding-and-cancer.info) And breastfed infants receive exposures to all of these toxins that are many times higher than formula-fed infants receive. (see Section 1 below)
There are undoubtedly health benefits to the mother of breastfeeding. As found in a 2010 Norwegian study, after a year of nursing, mothers’ breast-milk concentrations of PFCs, PBDEs, and PCBs (three major categories of developmental toxins) were reduced by 15−94%.(7b) Considering the amounts of those reductions that were taking place while the mother continued to be ingesting those toxins from the environment, the benefits to the mother are clear. The effects on the development of the small organism that was receiving the fully-grown person’s accumulations of those toxins, however, is a different question.
There is good evidence indicating that these toxins in breast milk are causing considerable harm. A U.S. study of all 50 U.S. states and 51 U.S. counties, carried out by a highly-published scientist and Fellow of the American College of Nutrition, found that "exclusive breast-feeding shows a direct epidemiological relationship to autism," and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism." Other, more local studies (in the U.S., Canada, and U.K.) have come to similar conclusions.(8) And despite the widespread belief that breastfeeding is beneficial for babies, strong evidence points in the exact opposite direction: Over 60 scientific studies have found that worse health outcomes were associated with breastfeeding or greater duration of breastfeeding, with at least 28 such studies in the categories of diabetes, asthma and allergies alone; those are in addition to many studies that have found no benefit of breastfeeding in areas in which benefits are claimed, including six in the area of SIDS alone. See www.breastfeeding-studies.info
Information about presence of harmful concentrations of toxins in breast milk will seem surprising to most people, given the widely-accepted view that breastfeeding is beneficial. In fact, there can be no doubt that breastfeeding was beneficial in earlier times; also, mothers in contemporary times whose diets are mainly vegetarian, as well as those who live in low-density, non-industrial regions, still have a good chance of producing low-toxin milk. The toxins contained in most present-day breast milk in developed countries have either originated as new chemicals in the environment in recent decades or have tremendously increased in the environments in the last half century or so. The toxins accumulate in animal tissues (mainly in fat) and "bio-magnify" at higher levels in the food chain, and therefore they are ingested very disproportionately by those at the top of the food chain (specifically those eating meat, dairy and fish). (Details and authoritative sources for all of this will be presented later in this article.) Likely effects of these toxins on developing brains of infants, with many examples of close correlations between highs and lows in breastfeeding rates and high and low levels of autism and childhood cancer, can be read about at www.pollutionaction.org/breastfeeding-and-autism-and-cancer.htm. A briefer look at correlations with specific regard to autism, considering mid-levels as well as highs and lows, and dealing with exposure and effects of mercury specifically, can be found at www.autism-correlations.info.
Atmospheric toxins (mainly products of combustion, including diesel emissions and tobacco smoke, and dusts emitted by electronic devices) are inhaled in far greater amounts by those who use computers, watch TV, smoke or live with smokers, and/or live in the more populated, high-traffic areas where such emissions are high; this contrasts with air quality in areas where most cows live and graze. Recent studies have also shown that autism rates are very disproportionately high among children of mothers who live in high-traffic, high-pollution areas, indicating that inhalation is also a major source of toxins' entering mothers’ bodies before being transmitted to their infants in harmful concentrations.
So it is essentially a matter of needing to update recommendations on breastfeeding to reconcile them with current realities in developed areas. Various studies have found benefits of breastfeeding, but the U.S. Surgeon General acknowledges that all of those studies are of the observational kind, which the U.S. Agency for Healthcare Research and Quality says are subject to false conclusion. (see link just below for sources on this and other points in this paragraph) There is excellent historical health data covering the period of transition from low breastfeeding rates to high breastfeeding (which took place mainly during the 1970's in the U.S.) which sheds considerable light on the real effects of breastfeeding; the many disorders that are alleged to be improved by breastfeeding have in every case but one actually worsened considerably since the transition to high rates of breastfeeding, as shown by government health data covering four decades. And the times, places, and demographic groups showing higher and lower levels of these disorders have been in fairly precise correlation with the times, places, and demographic groups showing higher and lower rates of breastfeeding. Full details and citations of authoritative sources regarding the points in this paragraph can be found at www.breastfeedingprosandcons.info. Also ADHD and serious psychological problems have greatly increased since 1972 (see www.breastfeeding-health-effects.info), as have developmental disabilities (see www.breastfeedingnegatives.info). Confirmed explanations for the several recent epidemics and major increases of childhood diseases have not been found, but the best explanation offered for several of them is the "hygiene hypothesis," according to which the recently-high levels of hygiene in developed countries have prevented many infants’ immune systems from receiving the stimulative challenges that would have enabled them to develop properly in earlier centuries. The highly-regarded immune cells in human milk, reducing an infant’s microbial exposure to levels even lower than what may already be too low in relation to developmental needs in many cases, should be seen in that light. For more information about the role of immune cells in breast milk as related to asthma and allergies, see www.breastfeeding-and-asthma.info. To read how the above matters relate to diabetes, see www.breastfeeding-and-diabetes.info.
This article will present evidence of near- and medium-term harm caused by toxins known to be contained in breast milk, since there has been little research on long-term harm resulting from those toxins. However, it should be kept in mind that, according to two experts in the field of developmental toxicology, "Developmental neurotoxicants may also cause silent damage, which would manifest itself only as the individual ages, and may contribute to neurodegenerative diseases such as Parkinson's or Alzheimer's diseases.”(9) Continuing, “a selected population of neurons may be affected, but the known plasticity of the brain would compensate for such loss. However, further exposure to exogenous influences (e.g., stress, disease, additional chemical exposure), or the natural aging process, would unmask the existing deficit."
The following is a summary of important points and section headings from the rest of this website:
Many-times higher infant intake of toxins from breast milk than from formula or from trans-placental exposure:
Section 1.a: Dioxins and PCBs, recognized neuro-developmental toxins, in doses scores to hundreds of times higher than in infant formula. "Significantly more (10 to 20 times) of a mother's body burden of persistent organohalogens is transferred to the infant via the milk than by the transplacental route."
Section 1.b: PBDEs, neuro-developmental toxins with potent estrogenic effects, almost 10 times higher in urban air than in rural air, and present in breast milk in concentrations over 30 times higher than in infant formula.
Section 1.c: Mercury, and brain development taking place after birth, Part 1: Mercury concentrations in infants that had been breastfed for one year were three times as high as those in infants that had not been breastfed; many studies finding associations of autism with mercury levels less than twice the normal range; over twice as much growth and development of the brain takes place in the year after birth as takes place before birth. Much more to follow in Section 1.d, including: Concentrations in human milk over 100 times higher than in infant formula.
Section 1.d: Development of the cerebellum (a key to autism), plus other postnatal vulnerability to toxins
Section 1.e: Specific mercury concentrations, breast milk vs. formula, and compared with a U.S. government maximum. More than 300,000 American newborns every year are considered by the EPA to already be at risk of neurological harm based on prenatal exposure alone, according to the EPA. Then, during a period of continued vulnerability of the rapidly developing brain to toxins, infants ingest either a food that could triple their mercury levels within one year (human milk) or a food that is less than 1% as high in mercury as the first alternative.
Immunological toxicity of different forms of mercury
Dramatic increases of mercury in modern times
Section 1.f Lead
A study of breastfeeding duration and infant blood lead reported that longer breastfeeding was associated with higher infant lead concentrations in three countries, in three different decades, in settings with differing breastfeeding patterns, environmental lead sources, and infant lead levels.
Section 1.g: Concentrations of other chemicals found specifically in human milk, compared with their concentrations in cows' milk or infant formula, including phthalates, perchlorate, PFOA, PFOS, pesticides, cadmium, aluminum, arsenic, manganese, and BPA
Section 1.h: Conspicuous effects of lactational exposure to developmental toxins, as opposed to effects only from gestational exposure: Studies finding harmful effects of toxic exposures that took place during lactation but not prenatally. Evidence of diseases’ incidences increasing in proportion to the duration or exclusiveness of breastfeeding.
Section 1.i: Breastfeeding and smoking
-- Breast-fed infants of smoking mothers have 10-fold higher exposure to smoking toxins than bottle-fed infants whose mothers smoke.
-- The American Academy of Pediatrics apparently believes in not telling the truth, at least on this subject.
Brief digression: There is a widespread assumption that infants are vulnerable to developmental toxins prenatally but have little postnatal vulnerability. That assumption has some validity as applied to most of the postnatal years, meaning after the first few years of life. But it is not at all valid in relation to the early-postnatal period, while very considerable development of the brain is still occurring, and when an infant’s ingestions of developmental toxins greatly increase in comparison with exposures during gestation. For considerably more detail on this subject, go to Section 2.a of www.pollution-effects.info.
Many-times higher infant intake of toxins from breast milk than from formula or from trans-placental exposure
For a summary of the data comparing toxins in breast milk versus in infant formula, citing sources, see Appendix B
To read about specific ways in which these toxins cause harm to infants, go to Section 2.a of www.breastfeeding-vs-formula.info.
As stated earlier, according to an EPA study, a typical contemporary breastfed U.S. infant ingests about 242 picograms (pg) of dioxin toxic equivalency (TEQ) per kg of body weight per day at initiation of breastfeeding. As the mother’s lifetime accumulation of these toxins is excreted in breast milk over the course of a year, the daily dose received by an infant gradually decreases to about 18 pg.(5) Findings in other developed countries have been in that same general range.(7) These figures should be compared with the dioxin concentrations in infant formula, as follows: A U.K. study, which appears to be the most thorough study on this subject, studied 96 samples of 32 different infant formula products and arrived at findings that it said were similar to results observed in other countries. According to their “upper bound” determinations (which they said were probably higher than actual concentrations) for 2003, almost all samples provided doses of 1.1 pg TEQ/kg body weight per day or less. Very compatible figures were found in a Dutch study of food consumed by non-breastfed children, adding in the toxicity equivalents also of PCBs as well as dioxins, and still only reaching 1.1 pg TEQ/kg body weight per day.(10) Data published in a UK official document indicated a figure of 0.3-0.4 pg TEQ/kg body weight per day.(10a)
Remember from above the doses in breast milk, for comparison.
According to the U.S. Agency for Toxic Substances and Disease Registry (ATSDR), ”PCBs (chemical relatives of dioxins, with many of the same properties) tend to accumulate in breast milk fat,” with accumulations increasing with the woman’s age. (11) A commission of the German Federal Environmental Office reported that the average daily intake of an adult is 0.02 micrograms of PCBs per kg of body weight, as compared with the intake of a breastfed infant, which is 3 micrograms per kg of body weight, or 150 times higher.(12) Other studies have observed that nursing infants consume a daily TEQ (toxic equivalency) intake that is 50 times higher than adults.(12b) A study in the Netherlands, also summarized by the ATSDR (p. 569), found that, even at 3½ years of age, the median plasma PCB levels of children who had been breastfed for a mere 6 weeks or more were still 4½ times as high as those of children who had been formula-fed. Patandin et al. (1999) reported a mean daily intake of 112–118 pg TEQ/kg bw in breast-fed infants, compared with only 6.3–6.5 pg TEQ/kg bw in typical 1- to 5-year-old children. A study published very recently (over 30 years after PCBs were banned from most manufacturing) showed PCB levels in 45-month-old children to be at 19 ng/g lipid for non-breastfed children vs. 60, 180, 309 and 365 for same-age children who had been breastfed for increasing durations (in 6-month intervals, up to 19 months plus).(12a)
Duration of breastfeeding has been found to be a significant predictor of child PCB levels even at age 14.(12d); 30% higher PCB levels were found among breastfed than among non-breasted youths at age 10-17.(12e) Dioxins are even more persistent than PCBs, as indicated by the following: In a 2011 study, by 13 scientists, it was determined that at ages18 to 26, average dioxin concentrations were still twice as high in the breastfed young men as in those who had been formula fed.(12f)
PCBs in human milk, even decades after their production was banned for most purposes in most developed countries, have been found to still be about 20 times the level allowed in U.S. public water systems.(12c)
In contrast with the high levels of PCBs found in breast milk, as indicated above, note that a study by scientists with the U.S. National Institute of Environmental Health Services examined 104 samples of infant formula and found no detectable PCBs in all but one sample.(10b)
It might seem that growing for nine months inside a mother's body would put a fetus at maximum vulnerability for exposure to toxins that had accumulated in the mother, but apparently that exposure can be minor compared with the effects of breastfeeding. According to what is apparently the most thorough study on the subject of infant absorption of toxins from mother's milk vs. from fetal absorption, "Significantly more (10 to 20 times) of a mother's body burden of persistent organohalogens is transferred to the infant via the milk than by the transplacental route." (Note that dioxins, PCBs and PBDEs are all included among organohalogen compounds.) Tests with animals have confirmed the above, with even higher ratios of lactational vs. transplacental transfer.(13) It should therefore not be surprising that many studies have found adverse health effects to be linked in dose-response relationships to varying amounts of breastfeeding; several have found adverse effects linked to exposure to toxins in breast milk while not finding effects from gestational exposure to those same toxins. (see Section 1.h) One such study, finding that gestational exposure to PBDEs (another chemical relative of dioxins) in mothers had no significant adverse effect, found that exposure to mothers' PBDE concentrations via breastfeeding was linked with an 80% increase in relative risk of attention-deficit problems and a 160% increased relative risk of poor social competence.(14)
A German study found that intake of dioxins was up to 50 times higher in breast-fed infants compared with formula-fed, and also that high proportions of the dioxins were intestinally absorbed by the breastfed infants. At 11 months of age, the dioxin toxicity-equivalent concentrations in the formula-fed infants were about 10 times lower than in the infants that were breast-fed for six to seven months.(15) EPA reports have stated similar findings.(16) However, the10-times-higher range of medium-term accumulation or concentration in the breastfed infants may understate the reality of the harm caused, since the much higher initial exposure may result in unusual harm during a brief period of maximum vulnerability, when a "window of sensitivity" for neurological development is likely to be taking place (see Section 1.2.b.1 at http://www.pollutionaction.org/breastfeeding-and-autism-and-cancer.htm.
The presence of these "persistent" toxins in the child's body declines after their rapid buildup during breastfeeding, but only very gradually. PCB levels in breastfed Dutch children at 42 months were found to be 3-4 times as high as in formula-fed children.(16a) The differences were even greater in an American study (although the mothers in that study had above-average exposure due to fish consumption): In 4-year-old children, body burden of PCBs in children breastfed for at least 6 months was found to be about 17 times as high as the burdens of those who had not been breast-fed (5.1 vs. 0.3 ng/ml).(16b) In an American/German study, PCB levels in children who had been breastfed merely for 12 weeks or more were still over twice as high as in bottle-fed children at 7 years of age.(17) Those are very substantial differences so many years after exposure, especially considering how much neurological development takes place during a child’s early years, and considering the amount of non-breastfeeding environmental exposure the children would have received during the intervening years following breastfeeding exposure.
As illustration of effects of PCBs, note the following: According to the U.S. Agency for Toxic Substances and Disease Registry, “there appears to be an overall consistency of effects among the human studies supporting sensitivity of the immune system to PCBs and these other chemicals, particularly in infants exposed in utero and/or via breast feeding.” The ATSDR also refers to “extensively corroborated findings in experimental animals that exposure to PCBs in utero and/or during early development (e.g., through breast milk) can deplete levels of circulating thyroid hormones in the fetus or neonate, which may give rise to a hypothyroid state during development; and (2) the recognition of the importance of thyroid hormones in normal development of the brain, as is evident from neurodevelopmental disorders and deficits associated with hypothyroidism.”(17a) Other authors are more specific about the duration of the period of harmful thyroid effects resulting from PCB exposure, stating that “thyroid hormone is essential for normal growth and development of the brain before birth and throughout infancy.(17b) A 2015 study by six scientists refers to “the extensive brain development that occurs postnatally, including cell differentiation that has been shown to be altered by PCBs….”(17b1)
For considerable additional evidence about adverse effects on children of postnatal exposure to PCBs, see Section 2.a of www.breastfeeding-vs-formula.info.
Studies published in 2013 and 2015 have found associations between autism and exposures to traffic-related and other atmospheric pollution, with especially strong associations of autism with air pollution exposures during the year after birth in a state (California) where long-term breastfeeding rates are especially high. This is relevant to this discussion because PCBs (as well as PBDEs and mercury) are known to be present in traffic-related pollution and particulate matter air pollution.(see www.air-pollution-autism.info).
Dioxins levels in human milk are quite sensitive to regional environmental exposures within the same countries. As stated in a year 2000 WHO publication, a “recent WHO human milk exposure study indicated that the daily intake in TEQs of PCDDs and PCDFs in breast-feeding infants in industrialized countries ranged from about 20 pg/kg bw in less industrialized areas to about 130 pg/kg bw in highly industrialized areas.”(17d) It would be reasonable to expect that exposures of most dairy cows would be similar to the exposures in less industrialized areas, and most humans in industrialized countries would have exposures that are typical of their countries.
Citing two earlier studies, a Dutch scientist states, “Literature data indicate that PCBs and dioxins are almost completely absorbed in the digestive tract of the breast-fed infant.” And also, “Milk lipids in formula are replaced by lipids mainly of vegetable origin, therefore the exposure to PCBs and dioxins of formula-fed infants is negligible.”(17e)
According to the EPA, “Studies on mice and rats have shown that exposure to PBDEs causes neuro-developmental toxicity, weight loss, toxicity to the kidney, thyroid, and liver, and dermal disorders…. Studies on animals and human beings have shown that some PBDEs can act as endocrine (hormone) system disruptors.”(18) And also, “One way chemicals can affect the brain is through disrupting the levels of thyroid hormones. These hormones help control the development and maturation of the central nervous system (the brain).”(19) “PBDEs… have been shown to interact as antagonists or agonists at androgen, progesterone, and estrogen receptors… most PBDEs have antiandrogenic activity… (many) BDEs have potent estrogenic activity… (some) have been shown to displace thyroid hormones…. “ (20) For more on developmentally-harmful effects of PBDEs, see www.child-disability.info.
In the EPA's 2010 Exposure Assessment of PBDEs, the only study quoted that measured typical U.S. infant intakes of PBDEs due to ingestion of mother’s milk found that to be 306 ng/kg/day (nanograms per kilogram of body weight per day);(21) another study, referred to by the NIH, concurred with that figure as an average but indicated a high end of the range in North America as 4100 ng/kg/day.(22) This compared with the EPA’s estimated total adult intake dose of 7.1 ng/kg-day.(23) This means that the average daily intake of a U.S. breastfeeding infant (according to the best available information) from mother's milk alone is over 40 times the average total intake of adults. That 306 ng/kg/day average, ranging up to 4100 ng/kg/day, should also be compared with the EPA’s Reference Dose (estimated relatively safe dose) of 100 ng/kg/day for the form of PBDEs that apparently constitutes over half of the PBDEs present in human milk and maternal serum (tetraBDE, or BDE-47).(18) (18a)) So it appears that infant exposures (at least in North America) range from well above the EPA’s estimated safe level (on average) up to over 20 times that safe level.
PBDEs in breastfed vs. bottle-fed children: In the only study quoted by the EPA making such a comparison, based on measurements of 244 children, the average total concentration of PBDEs in breastfed children at age four was still nearly three times as high (3.6 ng/g lwt) as in formula-fed children (1.3 ng/g lwt)(24). So the total concentrations of PBDEs resulting from four years of all postnatal exposure plus prenatal exposure was still almost three times as high in breastfed children as in formula-fed children. This is actually as should be expected, judging by the differences in PBDE concentrations found in infant formula vs. breast milk (over 30 to 1), as indicated by authoritative sources.(25) In line with the above, one study team calculated that 91% of a typical breastfed infant’s total exposure to PBDEs was from breast milk.(25a)
The huge difference between PBDE concentrations in human milk vs. cows' milk is due to
(a) the major presence of PBDE dust in residential and workplace interior air due to its use as a fire retardant in electronics and home furnishings; and
(b) the difference between urban air and rural air; according to a document of the U.S. Agency for Toxic Substances and Disease Registry, "The concentration of total PBDEs in air ranges from 5.5 pg/m3 in rural environments to 52 pg/m3 in urban air."(26) Presence of PBDEs in diesel emissions(27) no doubt helps account for this urban-rural difference. It should be born in mind that, as the term "urban" is likely to be used by government agencies, it includes most suburbs; according to the 2000 U.S. Census, 79% of the population lives in urban areas.(28) It is safe to assume that very few dairy farms and soybean fields (sources of alternatives to human milk) are located in such "urban" areas, just as it is safe to assume that cows and soybean fields have very little exposure to air around electronic devices and home furnishings.
An especially crucial consideration of PBDEs with regard to their probable effects related to recent increases of disorders and childhood epidemics: PBDEs have been dramatically increasing in modern environments in recent decades. (see Section 1.c.3 at www.breastfeeding-vs-formula.info). The increases have been especially rapid in North America. “Levels of PBDEs have significantly increased in the past decades, and those in human tissues in North America have been consistently found to be one to two orders of magnitude (10 to 100 times) higher than those reported in Europe and Asia.”(29) This has been true mainly because of previous U.S. regulations (California Technical Bulletin 117) that required the addition of flame retardants to prevent burn injuries and property damage (Sjodin et al. 2008).(28a)
Another reason why PBDE exposure is especially relevant to the increases in neurological disorders (especially autism) in recent decades: PBDE exposure has been associated in animal studies with increased death of cerebellar granule cells in the brain;(29a) this should be seen in combination with (a) the known major increase in PBDE exposure via lactation as compared with exposure during gestation,(29b) (b) the major increases that have been taking place in PBDE levels in breast milk in recent decades (see previous paragraph) and (c) the fact that dysfunction of the cerebellum has been implicated in many studies with autism.(see Section 1.d)
Although the neurodevelopmental toxicity of mercury has been most conspicuous in cases of accidental poisonings, there is also excellent evidence of neurological toxicity even in relatively common concentrations that are typical in modern environments. At least five published studies have found high levels of mercury in the autistic.(36) The many studies finding associations of autism or other adverse cognitive effects with mercury levels less than twice the normal range should be seen together with the findings from multiple studies of doubling or tripling of infant mercury levels resulting from breastfeeding: In a study by a prominent scientist (P. Grandjean) and his team, it was found that total mercury concentrations in infants that had been breastfed for one year were three times as high as those in infants that had not been breastfed.(33) This finding of rapid increase in infant mercury levels due to breastfeeding was very compatible with other information compiled by an EPA-contracted research group(34) and also with the over-200% increases due to 6 months of breastfeeding as found in another study.(35) See Figure 2 below and the text below it regarding the vulnerability of the infant’s neurological development during the period of breastfeeding.
Developmental toxicity of mercury has usually been thought of mainly with regard to the prenatal period, but there is ample evidence of its toxicity and its concentrated presence extending well into the postnatal period. Some of the studies finding adverse effects of mercury on infants have measured maternal mercury during pregnancy or at time of birth, and found poorer cognitive test scores later in children who had had higher mercury exposures that they called “prenatal;” but they said nothing to contradict the possibility that their measurements of maternal mercury levels might just as well indicate lactational exposures.(36a) Other studies have found associations of cognitive decline specifically with lactational or postnatal mercury exposures of children, as opposed to prenatal exposures.(36b) More growth and development of the brain takes place in the year after birth than takes place before birth, and many physiological processes involved in development of the brain take place after birth, so it should only be expected that harm could take place in either time period. (see Figure 2 below, and ”Other postnatal development of the brain,” below that in Section 1.d)
Observed effects of mercury contamination in human milk:
An international research group, studying growth of 182 children in the Faroe Islands, arrived at findings of relevance to this subject, showing physically-observable apparent effects of mercury and PCB concentrations in breast milk. The breastfeeding mothers and children in the Faroe Islands had well-above-average mercury exposure due to a high seafood diet, but the researchers pointed out that "exposure to seafood contaminants is a worldwide concern, and levels similar to or in excess of those recorded in the Faroes have been published from other communities with high seafood or freshwater fish intakes."(37) (italics added)
Is development of the infant brain especially harmed by methylmercury in human milk?
1) Methylmercury is one of the “environmental agents with the property of killing neurons as they are born,” according to a study referred to by the NIH and published in the journal, Environmental Health Perspectives.(38)
2) Rats exposed to methylmercury on postnatal day 7 were found to have brain cell death induced by one exposure to methylmercury at a level “that begins to approximate human exposure;” and this dose was “equivalent to a single daily exposure” at a level that is estimated to be chronic for many humans; this was according to a 2011 study published in the journal, Neurotoxicology, and referred to by the NIH.(39)
3) Methylmercury accumulates in the brain, and has been found to reach levels over seven times the levels in the blood.(40), (41) So, as a result of breastfeeding, a developing infant brain would sometimes be subject to a far greater concentration of methylmercury than the general level that produced the effects shown in Figure 1. Remember that this chemical is specifically known to kill neurons.
4) Observe in Figure 2 above that about 80% of the cerebellum’s normal growth takes place during the year after birth; also note (in the statement by EPA researchers in Section1.d just below) that an organ is generally at its greatest vulnerability to environmental toxicants if the exposure occurs during development of that organ. Then consider how closely this period of the cerebellum’s maximum vulnerability matches the period in which a typical breastfed infant would be ingesting high doses of mercury. Multiple studies have found neuronal abnormalities in the cerebellum in postmortem brains from people with ASDs.(41a) Also, the cerebellum has been found to be one of the two parts of the brain most affected by mercury.(42) Note that typical contemporary breast milk contains about four times the maximum level of mercury allowed in bottled water in the U.S., with many women having levels higher than this average figure (see “Specific mercury concentrations” below); this should be compared with what would probably be happening with a formula-fed infant, who would be ingesting less than 1% of that average amount of mercury.
5) PBDEs, the toxins that have been increasing especially rapidly in breast milk in recent decades, have also been found in a major experiment with rats to be neurotoxic “mainly in cerebellum.” The PBDE dose administered was so small that no behavioral effects were observed in the rats, but toxic effects were observed distinctly in the cerebella upon examination.(43)
After being aware of how typical toxins in breast milk are likely to harm development of the cerebellum during its period of maximum vulnerability, note the finding in several studies (see below) that the cerebellum has been found to be disproportionately underdeveloped among those with autism.
. . . . . . . . . . . . .
Comments or questions are invited: At the next link are comments and questions from readers, including six doctors. Some of the doctors have been critical but others have been in agreement with us (including one with children with health problems and one who says she has delivered thousands of babies); they put into briefer, everyday language and personal terms some important points that tend to be immersed in detail when presented in our own publications. Also, we have responded to many readers’ questions and comments, including about having breast milk tested for toxins and about means of trying to achieve milk that is relatively free of toxins, including the “pump and dump” option. To read the above, go to www.pollutionaction.org/comments.htm
. . . . . . . . . . . . .
Section 1.d Development of the cerebellum (a key to autism), plus other postnatal vulnerability to toxins
A 2013 study in the NIH’s National Library of Medicine generalized, based on many earlier studies, that “the cerebellum has emerged as a region of interest in autism studies because of converging findings from human postmortem research, human neuroimaging studies, and animal models…. Evidence appears to support cerebellar dysfunction… as a contributor to the autism phenotype.”(44) According to EPA researchers, an organ is generally at its greatest vulnerability to environmental toxicants if exposure to the toxins occurs during development of that organ.(45) (emphasis added) Being aware of the above, notice in Figure 4 that about eight times as much growth of the cerebellum normally takes place during the first year after birth as takes place prenatally. It is important to bear this in mind, since most research on developmental harm caused by mercury focuses almost entirely on prenatal exposures or on observations many years after birth, generally bypassing the critical early postnatal period. (Chart from Dobbing et al., Quantitative growth and development of human brain, Arch Dis Child, 1973 October: 48(10): 757-767 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1648530)
Then think about what would be by far the greatest source of toxins to the developing cerebella of many infants during that first year after birth: A Taiwanese study found that, of the three sources of infant mercury exposure, ingestion (breast milk), inhalation, and dermal exposure, 96 to 99.6% of the total mercury exposure was from breastfeeding.(32) Remember from Section 1.c that mercury has the “property of killing neurons as they are born,” and also note that typical breast milk contains a concentration of mercury several times higher than the maximum allowed in bottled water in the U.S. and over a hundred times higher than the average concentration in infant formula.(see Section 1.e below) But mercury is only part of the toxic exposure; remember from earlier in this article the extremely high levels of neuro-developmentally-toxic dioxins (and their chemical relatives, PCBs and the rapidly-increasing PBDEs) in human milk, compared with the EPA’s estimated safe levels and also compared with the doses in infant formula.
Several of the studies that focus on the cerebellum in connection with autism found (through neuro-imaging) that this organ was smaller in autistic than in non-autistic children.”(46) Remember from Figures 1 and 2 and the text below them that,
a) reduction in general growth after birth was linked in a very authoritative study to toxins ordinarily contained in breast milk; reduction in growth increased with each additional month of breastfeeding during the first six months; and
b) about 80% of the lifetime growth of the cerebellum would normally be taking place during an infant’s first year, a period in which a typical breastfed infant is ingesting (neuron-killing) mercury in doses over 100 times higher than would be ingested in infant formula.
Since many scientists have apparently adopted the general supposition that the only part of the “brain growth spurt” that is especially vulnerable to environmental contaminants is the prenatal part of that period, it is worth taking a second look at Figure 2 above; it should be obvious that by far the largest proportion of the brain’s rapid growth period takes place after birth. Related to that, remember the authoritative statement that an organ’s time of greatest vulnerability to toxins is while it is developing. Also of relevance is the following statement summarizing established knowledge about development of the brain: “At birth some cortical neurons are still migrating and many have not started to mature or differentiate… (they) are still in the process of extending axons and dendrites, developing dendritic spines, and forming synapses. The establishment of the myriad connections that characterize the mature brain is a continuing postnatal process….”(47) (emphasis added) Also see Section 1.h below concerning postnatal vulnerability of the developing brain.
The postnatal exposures that have received by far the most attention have been cases of actual poisoning or other high exposure, but there is good evidence that chronic low exposures are also harmful. A 2012 study (Xu et al.) stated that “our experiments together with previous studies warn against the potential effects of chronic low-dose mercury exposure,” finding that even low doses of mercuric chloride “caused a significant reduction in the rate of neuronal survival.”(42) Several studies have also found harmful neurological effects of low doses of mercury on adults.(47a)
So a typical infant brain in contemporary developed countries is going through what is probably its period of greatest vulnerability to environmental toxins at the same time as it is likely to be receiving at least three different toxins via breast milk (dioxins, PBDEs, and mercury), with each of those toxins typically being in doses that are well above the established safe levels, and in concentrations scores to hundreds of times higher than in infant formula.
Consideration of matters such as the above is particularly important in a period when, along with general increases in breastfeeding, there have been unquestioned (and unexplained) increases in ADHD and other neurodevelopmental disorders,(36) not to mention the apparently major increases in autism. There must be a reason for the findings in three separate studies (mentioned in the introduction) relating breastfeeding to autism, including the one by a highly-published scientist who concluded, based on a study of all 50 states and 51 U.S. counties, that “breast-feeding shows a direct epidemiological relationship to autism," with the relationship increasing in a dose-response relationship with the duration of breastfeeding.(8)
. . . . . . . . . . . . .
Specific mercury concentrations, breast milk vs. formula, and compared with a U.S. government maximum
The U.S. Agency for Toxic Substances and Disease Registry (ATSDR), based on the available information from various countries of the world, estimated that the mean concentration of mercury in breast milk of non-exposed women is 8 ppb (parts per billion) .(49) Notice that the above figure applied to people without unusual exposure to mercury; it is important to bear in mind that large numbers of people in the general population are in the more-exposed category, including many people working with art supplies, some who work in dental offices, recycling facilities or laboratories, those who live or work in buildings painted on the inside with mercury-containing latex paints or who use certain cosmetics, and many who live or work near or downwind from coal-burning power plants, municipal or medical incinerators, or waste disposal sites. (See Appendix))
The only readily-found survey of mercury in infant formula products (in Canada, 2003) found the average mercury level in milk-based, ready-to-use formula to be 0.028 ng/g (=.028 billionths of a gram per gram, or 0.028 ppb).(50) This is well below one percent of the mercury concentration in average breast milk, going by the best available data as quoted above.
Aside from fish and other seafood, the principal source of mercury in human bodies (other than the non-average exposures mentioned just above) is absorption of matter originating from dental amalgam, which is about 50% mercury. It should therefore not be surprising that products of cows and soybean fields do not have the mercury concentrations that are found in human milk. In addition: A study (Hapke, 1991) found that “cattle are able to demethylate mercury in the rumen and thus absorb less mercury; therefore, beef (meat) and cow's milk contained only 0.001–0.02 mg/kg (ppm) and 0.01 mg/kg (ppm) of mercury, respectively.”(50a)
The above data should be compared with the maximum mercury concentration allowed in bottled water, according to U.S. Federal Regulations: 2 ppb.(51) According to this standard, the average mercury level in milk-based formula tested in Canada (probably much the same as in the U.S.) is safe by a huge margin; but the mercury level in most human milk in developed countries greatly exceeds that maximum in most cases.
Numbers of American children vulnerable to neurological harm from mercury:
According to the EPA, it is estimated that more than 300,000 American newborns every year may have increased risk of learning disabilities associated with gestational exposure to methylmercury.(52) Bear in mind from above how high an infant’s exposure to mercury via breastfeeding is in relation to gestational exposure (a year of breastfeeding almost triples the infant’s mercury levels, relative to non-breastfed infants); also remember from Figure 2 above and the text below it how much development of the brain takes place during the breastfeeding period.
So hundreds of thousands of American newly-born infants are already at risk of neurological harm based on prenatal exposure alone, according to the EPA. Then, during a period of continued vulnerability of the rapidly developing brain to toxins, infants ingest either (1) a food (human milk)that could triple their mercury levels within one year (relative to non-breastfed infants),(33) or (2) a food that is less than 1% as high in mercury as the first alternative.
. . . . . . . . . . . . .
Effects of low doses of maternal mercury, only being observed years later at school age:
A document of the UN Environmental Programme reports that “a series of large epidemiological studies have recently provided evidence that methylmercury in pregnant women's marine diets,” at levels of maternal mercury that were only about one-tenth to one-fifth as high as doses that cause observed effects in adults, were found to have “subtle, persistent effects on the children's mental development as observed at about the start of the school age.” (53)
Toxicities and sources of various forms of mercury
Of the various forms of mercury, the form that is of the greatest concern for neurological development is methylmercury, according to the U.S. Agency for Toxic Substances and Disease Registry, referring to that chemical’s “accumulation in the central nervous system.”(40) As mentioned earlier, this toxin is one of the few “environmental agents with the property of killing neurons as they are born….”(38) It is another of the "persistent, bio-accumulative toxins" that increase greatly with each step up the food chain. The EPA says that "The most common way people in the U.S. are exposed to mercury is by eating fish containing methylmercury."(55) The inorganic form of mercury is also known to harm development of the brain (56), and that form enters the body mainly via dental amalgam. Mercuric chloride occurs widely in the environment due to its use as a fungicide, antiseptic, disinfectant, and other applications, often reaching into water supplies; a study by a team of seven researchers from the Department of Cell Biology and the Faculty of Medicine at the University of Calgary found that mercuric chloride “elicits detrimental effects on young, developing cortical neurons – ranging from reduced cell survival, impaired neurite outgrowth, compromised network assembly, to the degeneration of mature networks;” the researchers noted harmful effects when nerve tissue of experimental animals received exposures that the researchers referred to as “low.” They also state that mercuric chloride “is known to be five times as potent as MeHg (methyl mercury) in blocking L-type Ca2+ channels in hippocampal neurons.”(42) One doesn’t need to be familiar with what these “L-type Ca2+ channels” are in order to understand that a chemical that is unusually potent in its blocking of channels in brain cells is harmful. Elemental mercury vapor, which is found in the blood, is also known to have effects on the brain.(57)
So most (if not all) forms of mercury are neurodevelopmentally harmful, just in varying degrees.(57d) Even though measurements of concentrations may typically refer to unspeciated mercury, discussions of higher and lower levels of mercury are similarly relevant, especially since various species of mercury change from one form to another within the human body. Both organic and inorganic mercury are higher or lower in the body in direct relation to the number of amalgam fillings, which are made only from the inorganic form.(57a) The ethyl form of mercury (contained in the vaccine additive, thimerosal) has been found in studies not to be related to autism, but it may be significant that this chemical was very quickly removed from vaccines in the U.S. after medical authorities took up consideration of its possible effects. Other studies have also found no higher levels of neurological disorders in children with elevated levels of mercury, but those studies have either measured developmental effects too early to detect the major long-term effects of toxic exposures or else measured exposures far past the early-postnatal period of maximum vulnerability to such toxins (see Figures 1 and 2 and Appendix B of www.autism-research.net/postnatal-effects.htm)
The form of mercury typically used in most animal experiments is methylmercury, and mercury found in humans is normally not distinguished according to its species, but the two classifications are reasonably comparable; most of the mercury in human blood is methylmercury; among U.S. women with mercury concentrations in the highest 10% of those tested in the 1999-2000 NHANES survey, 92% of the mercury in their blood was found to be methylmercury.(57c)
Note the findings of two studies in which methylmercury was administered to infant rats at their age that was the neurodevelopmental equivalent of human time of birth, in doses that were at the high end of frequent human exposure; in both cases, that single dose produced “brain cell death,” and the damage was found in one study to be especially great in the hippocampus (important to memory function).(57b) Note that the doses administered in both of those studies were one-time doses, as opposed to daily doses at similar levels often ingested during breastfeeding.
Immunological toxicity of different forms of mercury:
“Experimental investigations show clearly that mercury compounds can have immunomodulating activity. Mercuric chloride and methylmercury inhibit most of animal and human lymphocyte functions…. These cells exhibit a greater sensitivity to the immunotoxic effects of methylmercury than to mercuric chloride.”(58) “An immunological effect has also been observed in studies on clinically asymptomatic workers with low level exposure” (to mercury); and “mercury can give rise to allergic and immunotoxic reactions.” (59) Signs of immunosuppressive effects were found in response to “very low doses of inorganic mercury.”(60)
A study of samples of mercury concentrations in marine animals showed average twelve-fold increases between the mid-to-late 19th century and the end of the 20th century. According to a 2004 publication on the website of the American Academy of Pediatrics, “increases in power plant emissions and industrial uses during the past 100 years have been accompanied by a 3-fold increase in environmentally available mercury. In these forms, mercury remains in the environment indefinitely.”(60a) Observation of a 700-year sequence of seabird eggshells from the South China Sea found that mercury levels increased steadily between 1800 and 2000, with a particularly rapid increase after 1970.(61) (Note that atmospheric mercury is known to travel around the world.) Using data for blood mercury levels in 6,174 women, ages 18-49, in the NHANES 1999-2006 data sets, it was found that inorganic mercury detection rose from 2% in 1999-2000 to 30% in 2005-2006.(62) According to a highly authoritative 2006 publication, mercury has been continuing to increase in the food chain.(62a)
Many people think of the fact that breast milk is the “natural” food for infants, and feel that it therefore should be the ideal food for infants, as indeed it was over most of human history. The only problem (as indicated in the environmental record just above) is that what was natural and beneficial over most of human history has been dramatically altered. The world has changed, and contents of human milk very much reflect some unfavorable aspects of the changes.
. . . . . . . . . . . . .
To sum up some preceding information:
Transfer of mercury to infants is apparently far greater by lactation than during gestation or via infant formula. Aside from mercury, 10 to 20 times as much of a mother's body burden of organohalogens (heavily present in diesel emissions) is transferred to the infant in breast milk as is transferred during gestation or in infant formula. (See Section 1.a above)
So both of the two specific pollutants that have been closely implicated with likelihood of autism become very greatly increased in the infant by breastfeeding.
Consider the above in relation to the fact that most of the brain's normal period of growth and development takes place (if it will ever take place) during the first year after birth (see Figure 2 and text below it).
Also consider all of the above in relation to the finding by a highly-published scientist and Fellow of the American College of Nutrition, concluding a U.S. study of all 50 U.S. states and 51 U.S. counties, that "exclusive breast-feeding shows a direct epidemiological relationship to autism" and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism."(63)
The medical establishment nevertheless recommends breastfeeding, because of its “recognized benefits.” But when the medical associations that recommend breastfeeding are questioned about the basis for their determination that breastfeeding is beneficial, they never respond. It isn’t because the questioning would be unduly burdensome to respond to: Below are the only two questions contained in the latest of three letters that have been sent over the past year to the American Academy of Pediatrics, American Academy of Family Physicians, American Congress of Obstetricians and Gynecologists, and the World Health Organization. No response has been received to any of the letters.
1) Can you give any reason to disagree with the following statement?
Breastfeeding has been found to be associated with adverse health outcomes in 51 scientific studies, including the largest study ever conducted on the health effects of breastfeeding; that was also the only study on this subject that has utilized randomization, which is the recognized best way to avoid the false conclusions that are often caused by confounders.1
2) Consider the following:
a) Typical U.S. breast milk of recent decades has been found to contain developmentally-toxic dioxins in doses over 100 times the EPA-estimated safe dose2 and also scores to hundreds of times higher than levels in infant formula;3 the breast-milk-vs.-formula disproportion is very similar with regard to mercury;3a
b) following the major increase in breastfeeding in the U.S. after 1971, four epidemics of childhood disorders came into being (diabetes, asthma, allergies and obesity); highs, lows and mid-levels of these epidemics have correlated closely with highs, lows and mid-levels of breastfeeding;4
c) a highly-published scientist, studying data from all 50 U.S. states and 51 U.S. counties, 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;"5
d) the four above-mentioned epidemics and the increases in ADHD and autism did not exist for the generation born in the 1950’s and 1960’s, for whom breastfeeding was unusual.4
e) all but one of the diseases said by Surgeon General Benjamin to be reduced by breastfeeding actually increased substantially after breastfeeding rates greatly increased in the 1970’s, according to CDC and other authoritative data.4
Q: Considering the above, how do you know that the undisputed high levels of developmental toxins in contemporary human milk are not having seriously harmful effects on children?
- (1) Three studies on the subject of breastfeeding and attention deficits and hyperactivity, 3 on the subject of breastfeeding and autism, 6 related to breastfeeding and obesity, 5 on breastfeeding and diabetes, 22 on breastfeeding and asthma or allergies, one relating breastfeeding to ear infections, and 11 studies that relate breastfeeding to developmental problems; not counted in the 51 total are 6 studies (which include a clear majority of the high-quality studies related to SIDS) that found no beneficial effect of breastfeeding on SIDS incidence; see www.breastfeeding-studies.info.
- (2) Infant Exposure to Dioxin-like Compounds in Breast Milk, Lorber (EPA senior scientist) et al., Vol.110, No. 6, 6/02, Environmental Health Perspectives, at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708 #Download, and EPA document at www.epa.gov/iris/supdocs/dioxinv1sup.pdf in section 4.3.5, at end of that section, regarding safe dose.
- (3) U.K. Food Standards Agency Food Survey Information Sheet 49/04 March 2004, Dioxins and Dioxin-Like PCBs in Infant Formulae, found at www.food.gov.uk/multimedia/pdfs/fsis4904dioxinsinfantformula.pdf
- (3a) see Section 1.c of this website (www.breastfeeding-toxins.info), above
- (4) For information about origins of major increases of all of the above in the U.S. in the 1970's when breastfeeding rates were rapidly increasing, see www.breastfeedingprosandcons.info.
- (5) Autism rates associated with nutrition and the WIC program. Shamberger R.J., Phd, FACN, King James Medical Laboratory, Cleveland, OH J Am Coll Nutr. 2011 Oct;30(5):348-53. Abstract at www.ncbi.nlm.nih.gov/pubmed/22081621
Any reader is invited to see if you can get a response to these questions from any organization or from any person who promotes breastfeeding. If anybody responds in writing, please send a copy of it to firstname.lastname@example.org or Pollution Action, 27 McWhirt Loop, Ste. 111, Fredericksburg, VA 22406 USA, since the organizations don't respond to us.
For more information on this matter, please visit www.breastfeedingprosandcons.info and/or
A printable one-page version of the above questions and footnotes is at www.breastfeeding-effects.info/Q.pdf .
If people in positions of authority are recommending to mothers that they feed their infants a substance that is known to contain very high levels of developmental toxins, at a time when there are several ongoing childhood epidemics that arose after that infant feeding increased greatly, shouldn’t those people be prepared to answer some questions about their recommendations? Obviously they should, but they never do.
Lead is sometimes given as an example of an environmental chemical that can be higher in infant formula than in breast milk, but those statements are based on findings of an earlier period, when formula typically came in cans sealed with lead. In more recent evidence, a U.S. Food and Drug Administration study for the period 2006-2011 investigated 34 samples of infant formula and did not find detectable levels of lead in any of the samples.(65a)
A study of breastfeeding duration and infant blood lead reported that longer breastfeeding was associated with higher infant lead concentrations in three countries, in three different decades, in settings with differing breastfeeding patterns, environmental lead sources, and infant lead levels. (65b)
There is good evidence indicating that elevated levels of lead in the mother are very effectively passed on to the infant in breast milk. In a Chinese study, the mean concentration of lead in breast milk of twelve occupationally-lead-exposed women was found to be “almost 12 times higher than that for the occupationally non-exposed population.”(66c)
In the only readily-found international comparison of lead levels in breast milk, the level in China was found to be two to 40 times as high as that in most other countries, with only Saudi Arabia being in near second place.(66g) It is for good reason that China imports a large amount of infant formula from New Zealand.
Considering the common presence of lead in cosmetics, it is not difficult to understand why milk even of mothers without special exposures would have significant levels of lead. The U.S. Food and Drug Administration had a survey done in 2010 analyzing lead contents of many different lipsticks purchased in retail stores, in which lead was found in all lipstick samples tested. The average lead content was 11 times the FDA’s recommended upper limit for lead in candy, but many lipsticks were far higher.(66b) A few examples:
Maybelline 125 Pink Petal -- 72 times the recommended maximum for candy;
L’Oreal 410 Volcanic -- 70 times the recommended maximum for candy;
Cover Girl Queen (Procter and Gamble) Ruby Remix-- 49 times the recommended maximum for candy;
L’Oreal 165 Tickled Pink -- 45 times the recommended maximum for candy;
Revlon 009 Fabulous Fig -- 32 times the recommended maximum for candy;
Avon 558 Mad for Mauve -- 31 times the recommended maximum for candy.
The FDA feels justified in allowing such lead contents in lipstick on the grounds that lipstick is intended for topical use, and is ingested in only small quantities. One might reasonably wonder whether a toxin in a substance covering the lips might not be ingested in more than insignificant quantities over the long term, considering its normal close contact with food and liquids crossing the lips, normal licking of the lips, and dermal absorption. Also, absorption of lead through the skin has been demonstrated experimentally in rats and in humans.(66j)
It is relevant to note the following quotation from Dr. David Bellinger, a professor of environmental health at Harvard’s School of Public Health, as follows: “No level of lead appears to be ‘safe’ (this is also the position of the CDC and the EPA) and even the current ‘low’ levels of exposure in children are associated with neurodevelopmental deficits (including reduced intelligence, poor academic performance, ADHD and anti-social behavior.)” (66h)
For much more on this subject, see www.breastfeeding-and-lead.info.
Perchlorate: Quoting from a 2005 study by a team of researchers at The Institute of Environmental and Human Health at Texas Tech University, “Perchlorate inhibits iodide uptake and may impair thyroid and neurodevelopment in infants…. Perchlorate in 47 dairy milk samples from 11 states and in 36 human milk samples from 18 states were measured…. The dairy and breast milk means were, respectively, 2.0 and 10.5 microg/L with the corresponding maximum values of 11 and 92 microg/L….The presence of perchlorate in the milk lowers the iodide content and may impair thyroid development in infant.” (68) Thyroid supply is especially significant because it is known to be important to neurological development.
It should be noted that California has a limit of 6 micrograms per liter for perchlorate in drinking water (68a1), which means that the average and especially the highest levels of perchlorate found in breast milk greatly exceed that limit.
A 2011 American study of perchlorate excreted by 206 infants estimated that breastfed infants had two to eight times the mean exposure to perchlorate compared with formula-fed infants, depending on type of formula; and many of the exposures were above the EPA’s reference dose (estimated relatively safe exposure level).(68) They said that their findings were consistent with the findings of four other (identified) studies. They also pointed out that the reference dose was based on a study of perchlorate’s effect on adults, without testing of infants, who are known to be much more vulnerable to the toxic effects because of their developmental stage.
Phthalates: These chemicals are widely present in contemporary plastic products, cosmetics, shampoos, skin moisturizers, vinyl flooring, building materials, detergents, insecticides, etc; they are known to have testosterone-reducing, de-masculinizing effects on males.(68a2) (also see Section 1.6.b of www.pollutionaction.org/breastfeeding-and-autism-and-cancer.htm) Bear in mind that testosterone is important to neurological development of infants (68a3). Two separate studies (of 130 and 36 samples) each found six different forms of phthalates present in 100% of breast milk samples.(68a)(68b) The most thorough study of phthalates in cows’ milk (7 samples tested) and infant formula (10 samples tested) detected only two forms of phthalates present; those two forms were found in lower average concentrations in cows’ milk and formula than were found in breast milk. (68b)
Some researchers seem to go on the assumption that only prenatal exposures to environmental toxins are likely to cause neuro-developmental toxicity. But, according to a study published in Environmental Health Perspectives in 2014, “Associations of early phthalate exposures with allergic asthma and reproductive and behavioural outcomes suggest that the fetus, neonate, and infant may be particularly vulnerable to endocrine disruptive effects of these compounds (Bergman et al. 2012; Bornehag and Nanberg 2010; Main et al. 2006; Miodovnik et al. 2011; Swan et al. 2005; Swan et al. 2010; Whyatt et al. 2012)."(68b1) Also, a Korean study found “a strong positive association between phthalate metabolites in urine and symptoms of ADHD” among 8-11-year-old children.(68c), and another study found similar results linking phthalates in U.S. school children with ADD and learning disabilities.(68f) Although these age groups were obviously well past the breastfeeding period, the findings nevertheless indicate a likely postnatal neurological influence of phthalates. This, combined with the apparently far higher levels of phthalates in human milk than in infant formula, may help explain why ADHD rose from not even being named as of the 1970’s to over 11% of the U.S. student population in 2012, with its growth following closely after the major growth of breastfeeding that occurred in the U.S. after 1971. (see www.breastfeeding-and-adhd.info).
In addition to the developmental harm apparently caused by phthalates, those toxins have also been found to be harmful in other ways. “In human studies of adults, phthalates have been related to decreases in sex steroid and thyroid hormone levels, poor sperm quality, endometriosis, insulin resistance, obesity, and possibly breast cancer.”(68d) A Danish study reported significant decreases in serum measures of free testosterone and Leydig cell function in 3 month-old boys in relation to phthalates in maternal breast milk.(68e) Concerning some of the just-mentioned substances that have been found to be reduced by phthalates exposure -- sex steroids, testosterone (which are produced by Leydig cells), and thyroid hormones -- note that all are known to be vital to neurological development; this may explain the association of phthalates with ADHD outcomes. (For more on this, see Section 1.a of www.breastfeeding-vs-formula.info). This relationship of phthalates with testosterone supply (and therefore with neurological development) could also help explain why ADHD, like autism, is especially high among males.
PFOA and PFOS are perflorinated chemicals that “are used in a wide variety of industrial and commercial products such as textiles and leather products; paper and packaging, coating additives, cleaning products, and pesticides”, according to the EPA. There are concerns about these chemicals’ “potential developmental, reproductive, and other systematic effects” as well as carcinogenicity. PFOAs are stated by the EPA to “cause developmental and other adverse effects in laboratory animals.” Like dioxins and PCBs, these chemicals are extremely persistent in the environment and build up in the human body.(69) But there is a way that women can greatly reduce their body burdens of these chemicals, as long as they don’t consider the consequences for their infants (yes, there are people who recommend breastfeeding at least in part because of its known effectiveness in cleansing a woman’s body of environmental toxins): Two different studies have found that women’s body burdens of PFOA are reduced by 94% or 60% during a year of breastfeeding. (That sounds good, so far) Another study estimated that breast milk contributed more than 94% and 83% of the total PFOS and PFOA exposure in 6-month-old infants.(70) Another study found that breastfed infants' levels of PFOA were doubled compared with those of their mothers, whereas bottle-fed infants had levels the same as their mothers.(70g)
After focusing on the many applications in which these chemicals are present (see first line of the previous paragraph), consider how much exposure cows have to these chemicals, as opposed to human mothers.
Pesticides: Quoting from a publication of the National Academy of Sciences, “Although pesticide application to some components of processed foods is likely to have occurred at some point (e.g., field applications to crops used as infant formula ingredients), measurements have consistently demonstrated that no pesticides are detected in finished infant formulas (Gelardi and Mountford, 1993). These invariably negative analytical findings are attributable to ingredient selection and processing procedures that reduce the potential for pesticide residues to appear in the finished product.”(70c) The U.S. Department of Agriculture in 2013 reported testing over 300 samples of infant formula and finding no detectable pesticide in 100% of dairy-based formula tested and in 99.4% of soy-based formula.(70d)
Apart from the extensively tested and observed absence of detectable levels of pesticides in infant formula, as reported by the above eminently authoritative sources, consider how heavily pesticides are used on human food crops, which are expected to be free of insect damage, versus how heavily pesticides would need to be used on cattle feed. (Bear in mind that pesticides and application equipment and labor all cost money, and their use would be determined mainly by how much the end user of the crop cares about insect damage.) In line with the above, at least two studies have found organochlorine insecticides (which include DDT) to be 20 times as high in human milk as in cow’s milk.(70a)
A Dutch study found some indication of the differences between prenatal and lactational exposures to pesticides, in line with protection provided by the placenta, as follows: “The very low concentrations of organochlorine (pesticide) in fetal blood prevented a study” that had been intended; however, about half of the mother’s estimated intake of DDT was estimated to be excreted by lactation.(70b) There was so little pesticide in fetal blood that it could not be studied, whereas half of a fully-grown person’s intake of DDT was channeled into a small infant by breastfeeding.
Although DDT was banned from use in most developed countries decades ago, it is still widely used in developing countries, especially for control of malaria. In a 2013 study in Ethiopia, it was found that “Mean levels of total DDT in the human and cow milk samples in the three areas were 12.68 and 0.389 μg g(-1) respectively.” And also, “the mean estimated daily intake of DDT by infants from mother's milk in the three locations was found to be 62.17 μg kg(-1) body weight, which is about three times higher than the acceptable daily intake set by WHO/FAO for total DDT, 20 μg kg(-1) of body weight.” By contrast, local cows’ milk would be within the acceptable daily intake by a very wide margin.(70e)
In a 2006 study in India, it was found that pesticide concentrations were ten times as high in breastfed infants as in bottle-fed infants after six months of breastfeeding.(70f) For more studies that have found far higher concentrations in breastfed infants than in bottle-fed, see Section 1.d of www.autism-studies.net For studies that have found average concentrations of DDT to be 19 times the acceptable daily intake (ADI) in India, and up to 100 times the ADI in Asia, see Section 2 at the above link.
For much more on this subject, see www.pesticides-and-breastfeeding.info.
Cadmium: Soy-based formula has been found to be much higher than breast milk in cadmium, but cow’s milk (and presumably cow’s-milk-based formula) is not. The only place in the website of the La Leche League that deals with cadmium says, “Cadmium levels in breast milk are about the same as in cow's milk.”(71) One study found cow’s milk to be lower than breast milk in cadmium.(72) A Canadian study found cadmium levels in milk-based formula to be “slightly higher” than levels in breast milk, but still well within the established safe range.(72a)
Aluminum: This metal is present in both breast milk and formula, apparently in higher average quantities in formula than in breast milk, but with considerable overlap in the ranges of exposure: the high end of the range of exposure in breast milk has been found to be over four times higher than the low end of the range of exposure in cows’ milk formula, according to a statement of the American Academy of Pediatrics.(72b) The type of formula that might be of reasonable concern is soy-based; the range of aluminum concentrations found in soy formulas is 6 to 33 times higher than that of cows’ milk formulas. (So that may be a good reason, along with others, to avoid soy-based formula.) The AAP statement continues, “A provisional tolerable intake recommended by the Food and Agriculture Organization of the United Nations and the World Health Organization is 1 mg/kg per day. Infants fed formulas with even the highest levels of aluminum … would receive an aluminum dose of less than 0.5 mg/kg per day.”(72b) Cows’ milk formula, with aluminum concentrations far below the levels that were themselves determined to be well within the safe range, is apparently especially well within the safe range.
The U.S. Agency for Toxic Substances and Disease Registry says, “It does not appear that children are more sensitive to aluminum than adults.“(72c) This contrasts with all of the toxins that are known to be present in breast milk in far higher concentrations than in formula (dioxin, PCBs, PBDEs, lead, mercury, perchlorate, and phthalates); all of those are either known or suspected to especially affect early development. (see earlier discussion) Also, four of those (dioxin, PBDEs, mercury and perchlorate) are all present in breast milk in concentrations normally far exceeding established safe levels, whereas infant formula has been found to be normally well within those safe levels.
Arsenic: This is a major exception to essentially all other toxins that are present in breast milk and formula, in that it is actually higher in formula than it is in breast milk. However, in what have apparently been the only two studies that tested infant formula and arrived at data expressed in the same terms used by the EPA to set the limit for arsenic in drinking water (10 mcg/L), the formulas that were highest in arsenic were far below that EPA limit, at 1.6 and 1.8 mcg/L. The highest levels were in rice-based formulas; it is recognized that rice in general is unusually high in arsenic.(72b1)
Manganese: Some studies have found much more manganese in infant formula and cows' milk than in human milk, but that is apparently negated by greater absorption of manganese from human milk. A 1989 study found that the total amount of absorbed manganese was insignificantly different between human milk, cow's milk, and infant formulas, except that it was significantly higher from non--iron-fortified cow's
milk formula (2 mg/L of iron) as compared with human milk.72b2
There appears to be confusion as to the desirability of extra manganese in milk for infants. A study published in 2017 found that twins with ASD have significantly lower levels of manganese than co-twins without ASD.72b3
BPA: BPA is another recognized endocrine disruptor, to which people including future mothers and nursing mothers are especially exposed via its use in plastic packaging of food and drinks, including in linings of metal cans; it has also been found to be transferred to humans from cash register receipts via dermal contact.(72c1) As with hundreds of other chemicals in modern environments (see www.breastmilk-pollutants.info), BPA has been found in most breast milk, according to the NIH. A 2013 study of BPA in early breast milk of 325 lactating women found the median level of BPA to be 7.8 ng/mL and estimated breastfed infant BPA levels to be about 10 times those of adults.(72e)
. . . . . . . . . . . . . . . . . . . .
The American Academy of Pediatrics lists the following cytotoxic drugs of concern in human milk: Cyclophosphamide, Cyclosporine, Doxorubicin and Methotrexate, all of which are implicated in possible immune suppression and carcinogenesis; also 12 drugs and chemicals reported in human milk "that have been associated with significant effects on some nursing infants," as well as 34 drugs that are listed as included in anti-anxiety, anti-depressant, anti-psychotic and other categories, which "could conceivably alter short-term and long-term central nervous system function" of the breastfed infant, and which are of "special concern" if the mother receives these medications over a long term.(73) Other toxic chemicals that are transferred from a lactating mother to an infant, as reported by the Pediatrics Academy, are from smoking and from drugs of abuse. (To read more about effects on an infant of breastfeeding combined with household smoking, and about the AAP’s vacillating position on this topic, see Section 1.i.) There are also many chemicals that are likely to be ingested by mothers through occupational exposure or from exposure to pesticides, dry cleaning chemical residue, medications, personal care products, household cleaning agents, paints, etc., before being transmitted in breast milk. One of those chemicals has been found in indoor air in 10 times higher concentrations than in outdoor air. As explained elsewhere in this article, mercury in breast milk is especially of concern; mercury compounds ”may be found in drugs for the eye, ear, nose, throat, and skin; in bleaching creams; as preservatives in cosmetics, tooth pastes, lens solutions, vaccines, … antiseptics, disinfectants, and contraceptives; in fungicides and herbicides; in dental fillings and thermometers; and many other products.”(74) One might wonder how many drugs like these enter the blood streams of cows, compared with the amounts to which human mothers are exposed.
Even a very condensed summary of the material concerning those chemicals, and their probable ingestion by nursing infants in hazardous quantities (as predicted by science professionals), is so long that it cannot be included here, but it can be found in the appendix.
One logical question that should come up is, "with all these harmful chemicals in human milk, wouldn't it taste bad to the infant?" It's partly a matter that the chemical that may be the most harmful of them, dioxin, is similar in properties to natural substances in human bodies, specifically the hormones that guide the infant's development. The main mechanism by which such toxins (“endocrine disruptors”) cause harm is by way of engaging with receptors in organs that ordinarily would be engaging with hormones from within the body. These receptors should be helping guide neurological development after receiving input from hormones; but instead of receiving normal signals from the body's own hormones, they are receiving other signals from similar-seeming (but foreign) substances. So harmfulness doesn't necessarily mean foreign taste.
But there are toxins of various different kinds contained in breast milk, in varying quantities according to the individual mother's exposure; and some of them might taste bad to the infant, which could explain why women and infants sometimes have difficulties in breastfeeding. For more on this topic, go to www.breastfeedingdifficulties.info .
“Neurotoxic effects of a number of environmental agents have been demonstrated in various studies, with critical windows of vulnerability to these agents occurring both pre- and postnatally.” This was according to researchers with the EPA’s National Health and Environmental Effects Research Laboratory (75); essentially the same statement was made by a large team of researchers in developmental neurotoxicology, mostly from the EPA, FDA, National Institute of Environmental Health Sciences, and two medical schools.(76) Describing the brain’s development, the highly-published expert in this field, Philippe Grandjean, also refers to “windows of susceptibility to hazardous agents at doses that might be totally innocuous to the mature brain. Any damage to this ‘wiring’ process can lead to brain damage…. Many of these processes continue until well after birth and some degree of vulnerability (to hazardous agents) therefore continues….” But he also refers to movement of neurons toward their final positions “shortly after birth,” a migration that is vulnerable to disturbances that would keep the neurons “from making proper connections with the neurons that should have been their neighbors.” (emphasis and parenthetical expression added)(77) Exposure of an infant to toxins should therefore be of particular concern if it takes place during the breastfeeding period, given that vulnerability of the developing brain to hazardous agents continues “until well after birth.”
Two leading experts on toxins involved in child development (Grandjean and Landrigan) have said, “Persistent lipophilic substances, including specific pesticides and halogenated industrial compounds, such as PCBs, accumulate in maternal adipose tissue and are passed on to the infant via breast milk, resulting in infant exposure that exceeds the mother’s own exposure by 100-fold on the basis of bodyweight.”(78) It is likely that prenatal exposure would be much closer to “the mother’s own exposure.” It is the concentration of toxins that takes place via lactation (combined with the brain’s continuing postnatal vulnerability) that causes an infant’s postnatal exposure via breastfeeding to be especially hazardous.
Reinforcing the above statement comparing breast milk toxins with the mother’s own exposure to toxins, remember from Section 1.a that organohalogens (which include dioxins and PBDEs) are transferred to infants via breastfeeding in 10 to 20 times greater quantities than are transferred during gestation; and exposure to mercury is also far greater after birth than before (see Section 1.c).
Regarding the special vulnerability of infants referred to by Dr. Grandjean as taking place “shortly after birth,” remember from the early paragraphs of this article that breast milk is especially high in dioxins soon after birth, having been found (in the U.S. and U.K.) to be initially hundreds of times higher in that neurodevelopmental toxin than the EPA’s estimated safe dose. One study, with support from another, arrived at a substantial figure for their estimate of the decline in a mother’s body burden of dioxins that takes place during 6 months of breastfeeding: 70%.(78b) The same initially-higher dosage, tapering off over the months as the mother’s accumulated burden of toxins is gradually excreted in her milk, also applies in the case of mercury.(see Section 1.c)
. . . . . . . . . . . . . .
Scientific studies indicating effects of specifically postnatal exposures to toxins of kinds heavily present in breast milk:
There have been good indications in scientific studies that certain effects of exposure to toxins occur only if transferred during lactation; the effects may not occur if similar exposure takes place via gestation. (See studies summarized below.) Remember from Figure 4 above and the accompanying text that the bulk of the brain’s growth takes place during the first year or so after birth and that an organ’s greatest vulnerability to toxins is during its development.
In addition to the cognitive effects of toxic exposure that have been found to occur especially and specifically after birth (to follow), it is well known that some exposures are very harmful both after and before birth. Lead may be the best-known example, and it is known that the infant brain is far more sensitive to the toxin than mature brains.(67) Note in Section 1.f that higher child lead concentrations have been found to be associated in at least two studies with breastfeeding as opposed to not breastfeeding, or associated with longer breastfeeding.
In addition to the lead example, one expert summarized previous PCB research as follows: “Several prospective cohort studies…have demonstrated that pre- and early postnatal exposure to PCBs is associated with deficit or retardation of mental and/or motor development, even after adjusting for maternal intelligence and developmental effects of the quality of the home environment.”(78a) It should be noted that high postnatal exposure to PCBs is essentially equivalent to breastfeeding exposure, given the findings of various studies (see Section 1.a), including the finding that PCB levels in breastfed infants were still 4½ times as high as in bottle-fed infants even at 3½ years of age.
A 2011 Spanish study found that gestational exposure to PBDEs in the mothers had no significant adverse effect on 4-year-olds, but exposure to those same mothers' PBDE levels via breastfeeding did have a substantial effect, including an 80% increase in relative risk of attention-deficit problems and a 160% increased relative risk of poor social competence.(79)
A Dutch study found a strong association of exposure to PCBs specifically via breastfeeding with problems with inattention and hyperactivity in children at 42 months after birth. The study distinguished between effects of prenatal and lactational exposure, and found that only the lactational exposure was associated with “less sustained attention” as well as slower reaction time.(80)
A large German research team found "negative associations between (human) milk PCB and mental/motor development ... at all ages." But they found no significant association of the children’s neurological development with PCB levels in umbilical cord blood.(81) However, they did find an association between the amount of PCBs in breast milk and developmental scores: as PCB concentrations in the mother’s milk increased from the 5th percentile to the 95th percentile, scores on the Bayley MDI decreased by 9.9 points.(82)
A study in Taiwan made distinctions between prenatal and lactational exposures to PCBs when investigating 236 four-year-olds. The researchers found that the highest lactational exposures (strongest among the offspring of women with above-average milk PCB levels who breast fed for at least 1 year) were “associated with reduced activity based on composite ratings provided by the child's mother and two independent examiners.” They said that this was an effect of high-level “lactation at contemporary levels of exposure.” (83)
Another Taiwanese study distinguished between prenatal and postnatal effects of methylmercury, and found no significant effects of prenatal exposure, but did find effects of postnatal mercury levels in three-year-olds, negatively correlating with scores in a test of expressive language. (83a) Bear in mind that language impairment is one of the traits of autism.
Another Taiwanese study summarized information regarding effects of PBDEs as follows: “Neonatal BDE-209 exposure has been demonstrated to have neurotoxic effects in most in vivo studies. Neonatal exposure to BDE-209 has been found to have developmental neurotoxicity, including hyperactivity; learning and memory defects; a reduction in habituation; a decrease in hippocampal nicotinic receptors; changes in spontaneous and cognitive behaviors; a change in locomotor activity;…. The results of this study show that infants exposed to BDE-209 probably experience developmental delays in cognition.”(98)
A study of cognitive effects of “Postnatal Exposure to Methyl Mercury” did not specifically investigate lactational exposure, but it did research effects of postnatal exposures. This study found that “In the primary analysis at 107 months there were four postnatal associations present. All were in the direction of declining performance as (postnatal) exposure increased.”(47) Remember from Section 1.c that (a) mercury concentrations are typically over 100 times higher in breast milk than in infant formula, (b) that breast milk is therefore the overwhelmingly predominant source of exposure to mercury during the period that is especially vulnerable to toxins, (see Figure 4 and accompanying text) and (c) that mercury persists in the body.
In a study supported by both the NIH and the European Commission, the authors stated that “TCDD (dioxin) and (the related chemical) dioxin-like PCBs have well-established effects on the immune system, one of which is thymic atrophy, an outcome observed in all species evaluated after TCDD exposure.”(85) (The thymus “is necessary in early life for the normal development of immunologic function.” (Farlex Partner Medical Dictionary)) In their study of over 900 Slovakian mother-infant pairs, these investigators observed that maternal PCB concentration (therefore prenatal exposure of the infant) had no correlation with the size of the thymus at 6 or 16 months of age; but the infant’s PCB concentration at 6 months of age was associated with a significant decrease in the size of the thymus at that age. The effect of PCBs in reducing the size of the thymus at the 6-month point was so substantial (in relation to the smaller size reduction associated with prenatal exposure to PCBs) that the authors concluded that their “results suggest that 6 months of age is … the period of greatest sensitivity to PCBs.” They pointed out that this finding of distinctly postnatal sensitivity of the thymus to toxins was also observed in other studies.(85) Being aware of the special first-year postnatal vulnerability of the gland that is necessary for development of immunological function, remember from Section 1.a that PCB levels in children who had been breastfed for at least 12 weeks were found to be still over twice as high as in bottle-fed children even at 7 years of age.
A relationship between PBDE measured in breast milk, but not placenta, and risk of cryptorchidism was reported in a Danish case-control study of 95 cryptorchid boys.(85a)
Remember from Section 1.g above (Phthalates sub-section) that phthalates exposure is apparently much higher in breast milk than in formula, and that (postnatal) concentrations of phthalates in school children were found to be associated with ADHD and learning disabilities; and also that reduced testosterone (important to brain development) was found in 3-month-old infants in relation to higher levels of phthalates in breast milk. All of those findings of apparent harmful postnatal (including lactational) effects of phthalates should be seen together with the finding in at least one study that prenatal exposure to phthalates (judging by the maternal urinary concentrations) did not have a significant general effect on test results of the infants at 2 and 3 years of age.
For much more on the subject of vulnerability of the developing brain to postnatal toxic exposures, see www.autism-research.net/postnatal-effects.htm.
Evidence of diseases’ incidences increasing in proportion to the duration or exclusiveness of breastfeeding:
If a study finds that incidence of a disease increases in proportion to the duration of breastfeeding, that provides especially strong evidence that the outcomes result specifically from lactational exposure to toxins.
Asthma: "For children with maternal asthma, the percent developing active MD asthma increased significantly with longer duration of exclusive breastfeeding."(86)
A study of children in the Faroes Islands, published in 2010, found that risk of allergy development increased with each additional month of breastfeeding.(87)
In a 2011 U.S. study of 739 children up to age 6, increases in allergies found to be associated with breastfeeding were quite large and were greater for children who were breastfed for longer durations.(88)
In a 2011 Taiwan study of 18,733 babies, it was found that, "After adjustment for potential confounders, the overall results showed that the increased duration of breastfeeding seemed to increase the risk of AD (atopic dermatitis) at 18 months in children.(89)
In a 2005 New Zealand study of 550 children at 3½ years of age, it was found that the odds ratios of developing atopic dermatitis increased from 1 to 6.1 to 9.7 as the children’s feeding histories went from (a) never breastfed, to (b) less than 6 months of breastfeeding, to (c) more than 6 months of breastfeeding.(90)
In a 2012 Australian study of peanut allergy in 15,142 school children, it was found that the odds ratios of developing the allergy progressively increased from 0.63 to 0.83 to 1.43 as the categories of the children’s infant feeding went from (a) those fed only foods other than breast milk before six months, to (b) those who were partially breastfeed, to (c) those who were exclusively breast fed. The authors also noted that other research concurred with theirs, in finding that the odds of developing peanut allergy were almost three times higher when comparing children who had had prolonged breastfeeding with children weaned at or before 6 months.(91)
In a German study of 1314 infants born in 1990, analyzing the effect of any breastfeeding duration on the prevalence of atopic eczema, it was found that the prevalence of atopic eczema in the first seven years increased with each additional month of breastfeeding.(92)
Study finding impairment of children to vary according to concentration of toxins in breast milk: A 2012 study, of effects of PBDEs in breast milk, found that children who had consumed breast milk with first and second quartile levels of the predominant form of PBDEs showed over three and two times the likelihood of later having ADHD, based on behavior test scores, compared with children who had consumed breast milk with below-median levels of PBDEs. (95)
Cognitive Development: A 2012 study reported that its "findings suggest an association between PBDE concentrations in colostrum (early breast milk) and impaired infant cognitive development." The authors also pointed out that “in the group of children breastfed for a longer period the association between BDE-209 exposure and neuro-development impairment was somewhat stronger….”(94) And “further, associations in the longer breastfeeding group may be underestimated because the higher social class and education level of these mothers may provide a more advantageous environment for neuro-development.”
Autism: A U.S. study of all 50 U.S. states and 51 U.S. counties, carried out by a highly-published nutritionist and Fellow of the American College of Nutrition, 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." (93)
Studies finding long-term effects of exposures of infant animals to environmentally-relevant doses of PCBs, PBDEs and mercury:
There is excellent evidence from animal studies (including primates) that early postnatal exposure causes later cognitive deficits. In a study by a researcher with Health Canada’s Bureau of Chemical Safety, provided in the NIH’s National Library of Medicine, assessing “the behavioral consequences of postnatal exposure to PCBs,” monkeys were dosed from birth to 20 weeks of age with a PCB mixture representative of the PCBs typically found in human breast milk, in environmentally-relevant doses. When tested, the performances of the treated monkeys were “much less efficient” than those of the controls, and they remained that way during 51 sessions of the test; the author concluded that the test provided “further evidence that PCB exposure limited to the early postnatal period and resulting in environmentally relevant body burdens produces long-term behavioral effects.” (96) Another study, administering PBDEs to dams of suckling newborn rats and later to the infant rats in chow, in doses that mimicked low-level chronic human exposure, found that when tested in adulthood the rats “demonstrated significant impairments in sustained attention and inhibitory control, as evidenced by increased premature responding and decreased accuracy of responding.”(97)
According to an EPA document, “All of these observations (from multiple studies) are consistent with a hypothesis that either developmental or adult exposure to methylmercury can have adverse long-term sequelae that may not be detected for years or decades following cessation of exposure.”(97a)
When reading about effects of “early postnatal” or “neonatal” exposures to PCBs and PBDEs, it should be remembered that those exposures are to a great extent lactational exposures, given that
a) (according to the only available data) human milk is typically over 50 times higher in PBDEs than formula.(24), (25) and
b) at 3½ years of age, the median plasma PCB levels of children who had been breastfed for only 6 weeks or more were still 4½ times as high as those of children who had been formula-fed. (see beginning of Section 1.a)
Referring to the “striking deficits in several cognitive tasks” on the part of animals postnatally treated with PCBs in doses similar to those in human breast milk, as well as to findings of other studies, authors writing in Environmental Health Perspectives pointed out probable reasons why similar effects were not found in some studies of human children: the mothers of the breastfed children were known to have been more highly educated, with higher IQs, and provided more stimulating home environments, all of which would have been expected to provide upward bias in tests of the breastfed children, canceling out the negative effects of PCBs in their milk.(99) Studies mentioned earlier in “Studies finding harmful effects of toxic exposures that took place during lactation” also provided strong evidence of harmful effects on human children of postnatal exposure to PCBs and other toxins.
. . . . . . . . . . . .
Knowing that the American Academy of Pediatrics (AAP) is concerned about lactational transfer of toxins from tobacco smoking to infants (see below), it is relevant to note that a 1998 study (of 330 mother-infant pairs) found that "breast-fed infants of smoking mothers have urine cotinine levels 10-fold higher than bottle-fed infants whose mothers smoke."74a (Cotinine is a marker for smoke exposure) This provides additional confirmation that lactation is a highly-efficient mechanism for taking in environmental toxins in moderate doses and transferring them to infants in highly-concentrated form.
Shown below is an AAP chart showing smoking to be one of “Drugs of Abuse” that the AAP considered to be contraindicated during breastfeeding. (Aside from the effects of smoking while breastfeeding as mentioned in the chart, note that childhood cancer is relatively high in the early postnatal period --see Figure 1 in www.breastfeeding-and-cancer.info)
It is interesting to note that the most recent position statement of the AAP on this subject no longer shows nicotine/smoking as a drug that is contraindicated during breastfeeding; that is somewhat surprising, since they make no mention of any new evidence showing that the “hazardous to the nursing infant” description shown above is any less valid now than it was earlier. As indicated under the above chart, the AAP “strongly believed” earlier that smoking should not be combined with breastfeeding, and they show no basis for a change in that position. But they now withhold that still-valid statement. Their explanation for why they no longer contraindicate smoking during breastfeeding is the rather revealing statement, “The Committee on Drugs wishes to support the emphasis of the American Academy of Pediatrics on increasing breastfeeding in the United States.”(74b) The AAP feels that it is important to withhold from the public fully-valid information about when breastfeeding is known to be harmful. So, rather than enabling doctors and parents to learn about all important considerations that apply to breastfeeding, the AAP relegates information such as shown in the above chart to an archive where extremely few people would go to the effort to find it. What does that say about the strength of their case, if they feel a need to conceal relevant, undisputed evidence that conflicts with their latest position?
But the above is only the beginning of the AAP’s withholding of important evidence in this matter. There are over 50 published, peer-reviewed studies that have found adverse effects of breastfeeding (see www.breastfeeding-studies.info), none of which the AAP mentions in their position statement that promotes breastfeeding.(74c) They do not deny the validity or question the quality of those negative studies when they are pointed out to the AAP (in letters from the author of this article). They just don’t want parents or doctors to find out about them. When it is pointed out to them that the infant feeding that they are promoting contains extraordinarily high levels of neurological toxins, at levels far exceeding established safe levels and also far higher than in alternative feedings, (see Sections 1.a, 1.b and 1.c above) they also do not deny that. They just don’t want people to be aware of it.
. . . . . . . . . . .
Since many negative considerations about breastfeeding are being pointed out here, we should provide at least the following concerning the major alternative to breast milk: a link to guidance in choosing which infant formula to feed an infant. There is a good section on that in the website of Healthy Child Healthy World, at http://healthychild.org/easy-steps/find-safer-baby-formula. (That organization, in line with widespread opinion, encourages breastfeeding as the preferred feeding method.)
. . . . . . . . . . .
Because of lack of additional space at this location, the general discussion of toxins in breast milk and formula is continued on a separate website, at www.breastfeeding-vs-formula.info. Following is the table of contents of that website:
Section 1: Dioxins, PBDEs, PAHs and BPA acting as Developmental Toxins (Endocrine Disruptors), Carcinogens, and Mutagens
- ADHD-like effects of PBDEs
- PBDEs as autism risk factors
Section 1.b: Sources of these toxins
Section 1.c: Typical breast milk these days is very different from that of earlier times
1.c.1 Increases of Dioxins -- PCBs
1.c.2 Increases in mercury
1.c.3.a 100-fold increase in human exposure to endocrine-disrupting BPA (Bisphenol A)
1.c.4 Diesel emissions and inhalation of toxins in developed areas
Section 2: More on how these toxins harm development
2.a: Exclusions and deletions of information that matters
Section 3: Synergistic effects resulting from combined exposures to multiple toxins at low doses in breast milk
Message to health professionals and scientists reading this paper: This author cordially invites you to indicate your reactions to the contents presented here. As of now, new parents almost never hear anything but completely one-sided promotion of breastfeeding, with no mention of possible drawbacks except in cases of serious problems on the part of the mother. If you feel that parents should be informed about both sides of this question and thereby enabled to make an educated decision in this important matter, please write to the author of this paper. Also, if you find anything here that you feel isn't accurately drawn from trustworthy sources or based on sound reasoning, please by all means send your comments, to email@example.com.
Comments or questions are invited. To read comments and questions from six doctors and from a number of readers, and for the link for sending in your own comments or questions, go to www.pollutionaction.org/comments.htm . We already know that many people don’t like the general gist of what we are saying, so don’t bother telling us that. But specifics are welcome. Also, note that we don’t feel obligated to present the favorable side of the breastfeeding debate, since that is already very amply (and one-sidedly) presented in many other, widely-distributed publications.
* About Pollution Action and the author of this publication: Please visit www.pollutionaction.org
(1a) Di Renzo et al., International Federation of Gynecology and Obstetrics opinion on reproductive health impacts of exposure to toxic environmental chemicals, International Journal of Gynecology and Obstetrics, 2015, at http://www.figo.org/sites/default/files/uploads/News/Final%20PDF_8462.pdf
(4). At http://www.epa.gov/iris/supdocs/dioxinv1sup.pdf in section 4.3.5, at end of that section, "...the resulting RfD in standard units is 7 × 10−10 mg/kg-day." (that is, O.7 pg of TEQ/kg-d) In the EPA’s “Glossary of Health Effects”, RfD is defined: “RfD (oral reference dose): An estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure of a chemical to the human population (including sensitive subpopulations) that is likely to be without risk of deleterious noncancer effects during a lifetime.”
(5). Infant Exposure to Dioxin-like Compounds in Breast Milk Lorber (Senior Scientist at EPA) and Phillips Volume 110 | Number 6 | June 2002 • Environmental Health Perspectives (a peer-reviewed journal published by the National Institute of Environmental Health Sciences of NIH) http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download
U.K. Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment: COT Statement on a toxicological evaluation of chemical analyses carried out as part of a pilot study for a breast milk archive, 2004, Table 1 and item 41, at http://cot.food.gov.uk/pdfs/cotsuremilk.pdf
Yang J, et al., PCDDs, PCDFs, and PCBs concentrations in breast milk from two areas in Korea: body burden of mothers and implications for feeding infants. Chemosphere. 2002 Jan;46(3):419-28. Found at http://www.ncbi.nlm.nih.gov/pubmed/11829398
Also: Bencko V et al., Exposure of breast-fed children in the Czech Republic to PCDDs, PCDFs, and dioxin-like PCBs. Environ Toxicol Pharmacol. 2004 Nov;18(2):83-90. doi: 10.1016/j.etap.2004.01.009. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/21782737/
Also: Focant et al., Levels of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and polychlorinated biphenyls in human milk from different regions of France, Science of The Total Environment, Volumes 452–453, 1 May 2013, Pages 155–162 abstract at http://www.sciencedirect.com/science/article/pii/S0048969713002404
Also: Costopoulou, Infant dietary exposure to dioxins and dioxin-like compounds in Greece, Food and Chemical Toxicology Volume 59, September 2013, Pages 316–324, at http://www.sciencedirect.com/science/article/pii/S0278691513003803
Also: Nakatani T, et al., Polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and coplanar polychlorinated biphenyls in human milk in Osaka City, Japan Arch Environ Contam Toxicol. 2005 Jul;49(1):131-40. Epub 2005 Jun 22. Found at http://link.springer.com/article/10.1007%2Fs00244-004-0051-y#page-1
Also: Deng B, et al., Levels and profiles of PCDD/Fs, PCBs in mothers' milk in Shenzhen of China: estimation of breast-fed infants' intakes.Environ Int. 2012 Jul;42:47-52. doi: 10.1016/j.envint.2011.03.022. Epub 2011 Apr 30. At http://www.ncbi.nlm.nih.gov/pubmed/21531025
Also: Li J, Zhang L, et al., A national survey of polychlorinated dioxins, furans (PCDD/Fs) and dioxin-like polychlorinated biphenyls (dl-PCBs) in human milk in China. Chemosphere. 2009 May; 75(9):1236-42. doi: 10.1016/j.chemosphere.2009.01.073. Epub 2009 Feb 28. At http://www.ncbi.nlm.nih.gov/pubmed/19251302
And also: Chovancová J, et al., PCDD, PCDF, PCB and PBDE concentrations in breast milk of mothers residing in selected areas of Slovakia Chemosphere. 2011 May;83(10):1383-90. doi: 10.1016/j.chemosphere.2011.02.070. Epub 2011 Apr 6. At http://www.ncbi.nlm.nih.gov/pubmed/21474162
And also: J Grigg, Environmental toxins; their impact on children’s health, Arch Dis Child 2004;89:244-250 doi:10.1136/adc.2002.022202 at http://adc.bmj.com/content/89/3/244.full
(7a) Pietrzak-Fiećko et al., Polychlorinated Biphenyls in Human Milk, UHT Cow’s Milk and Infant Formulas, Polish Journal of Environmental Studies Vol. 14, No. 2 (2005), 237-241 at http://www.pjoes.com/pdf/14.2/237-241.pdf
(7b) Thomsen et al., Changes in Concentrations of Perfluorinated Compounds, Polybrominated Diphenyl Ethers, and Polychlorinated Biphenyls in Norwegian Breast-Milk during Twelve Months of Lactation, Environ. Sci. Technol., 2010, 44 (24), pp 9550–9556, at http://pubs.acs.org/doi/abs/10.1021/es1021922
(8). Autism rates associated with nutrition and the WIC program. Shamberger R.J., Phd, FACN, King James Medical Laboratory, Cleveland, OH J Am Coll Nutr. 2011 Oct;30(5):348-53. Abstract at www.ncbi.nlm.nih.gov/pubmed/22081621 The full text, including the quoted passages, can be purchased for $7 or reference librarians at local libraries could probably obtain it at no charge. Other studies finding disproportionately high autism rates among more-breastfed children include the following:
Breastfeeding and Autism P. G. Williams, MD, Pediatrics, University of Louisville, and L. L. Sears, MD, presented at International Meeting for Autism Research, May 22, 2010, Philadelphia Marriot, found at https://imfar.confex.com/imfar/2010/webprogram/Paper6362.html)
- Dodds et al., The Role of Prenatal, Obstetric and Neonatal Factors in the Development of Autism, J Autism Dev Disord (2011) 41:891–902 DOI 10.1007/s10803-010-1114-8, Table 6, at http://autism.medicine.dal.ca/research/documents/2011DoddsetalJAutDevDisord.pdf This 2010 Canadian study, drawing data from a population-based “clinically-rich perinatal database,” investigated a very large population, nearly 130,000 births. Data from almost 127,000 of those children (those without identified genetic risk of autism) went into the study’s finding that there was a 25% increased risk of autism among children who were breastfed at discharge from the hospital.
- Whitely et al., Trends in Developmental, Behavioral and Somatic Factors by Diagnostic Sub-group in Pervasive Developmental Disorders: A Follow-up Analysis, pp. 10, 14 Autism Insights 2009:1 3-17 at http://www.la-press.com/redirect_file.php?fileId=2425&filename=1725-AUI-Trends-in-Developmental,-Behavioral-and-Somatic-Factors-by-Diagnostic-.pdf&fileType=pdf This study found that 65% of autism cases had been breastfed for a certain period; the authors looked at a comparison figure of 54%, but that figure was unrealistically high, since it came from a study (Pontin et al.) of breastfeeding by mothers largely from “more affluent families”, who breastfeed at unusually high rates in the U.K. For breastfeeding prevalence data that would apply to the general U.K. population, the authors of the Pontin study referred the reader to Infant Feeding 1995 (Foster et al.); examination of the data in that book reveals that a figure in the upper 20%’s would apply for the equivalent period (just after four weeks). That is also as was found in the U.K. Infant Feeding Survey - UK, 2010 Publication date: November 20, 2012, Chapter 2, at http://www.hscic.gov.uk/catalogue/PUB08694/ifs-uk-2010-chap2-inc-prev-dur.pdf
(9). Gennaro Giordano and Lucio G. Costa1 , Developmental Neurotoxicity: Some Old and New Issues ISRN Toxicol. 2012; 2012: 814795. Published online 2012 June 24. doi: 10.5402/2012/814795 PMCID: PMC3658697
(10). U.K. Food Standards Agency Food Survey Information Sheet 49/04 MARCH 2004, Dioxins and Dioxin-Like PCBs in Infant Formulae, found at http://www.food.gov.uk/multimedia/pdfs/fsis4904dioxinsinfantformula.pdf
Compatible figures were found in a study at Chemosphere. 2006 Aug;64(9):1521-5. Epub 2006 Jan 25. Weijs PJ, et al., Dioxin and dioxin-like PCB exposure of non-breastfed Dutch infants.
(10a) U.K. Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment: COT Statement on a toxicological evaluation of chemical analyses carried out as part of a pilot study for a breast milk archive, 2004, Table 1, at http://cot.food.gov.uk/pdfs/cotsuremilk.pdf
(10b) Rogan et al., Polychlorinated Biphenyls (PCBs) and Dichlorodiphenyl Dichloroethene (DDE) in Human Milk: Effects of Maternal Factors and Previous Lactation, American Journal of Public Health, A1JPH February 1986, Vol. 76, No. 2, in "Chemical Levels" section, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1646471/pdf/amjph00265-0062.pdf
(12). Kommission “Human-Biomonitoring” des Umweltbundesamtes: Stoffmonographie PCB - Referenzwerte für Blut (Commission on Human Bio-Monitoring of the (German) Federal Environmental Office: Substance Monograph on PCB - - Reference Values for Blood) At http://www.umweltdaten.de/gesundheit/monitor/pcbblut.pdf , Section 8.3. found within http://www.umweltbundesamt.de/gesundheit/publikationen/index.htm , website of Umwelt Bundes Amt (German Federal Environmental Office). This article cited for this breastfed infant exposure data the source: Institut für Wasser-,Boden und Lufthygiene des Umweltbundesamtes, Kommission „Human-Biomonitoring“ des Umweltbundesamtes • Berlin: Referenzwerte für HCB,b-HCH, DDT und PCB in Frauenmilch (Institute for Water-, Soil and Air Hygiene of the Federal Environmental Office, Commission on Human Bio-Monitoring: "Reference Values for HCB,b-HCH, DDT und PCB in Human Milk." The text drawn on says, " "Die derzeit durchschnittlich vom Erwachsenen täglich aufgenommene Menge an PCB (ca. 0,02 μg PCB/kg KG ) liegt deutlich unter der ATD von 1 μg PCB/kg KG. Der gestillte Säugling erhält dagegen eine deutlich höhere PCB-Zufuhr (3 μg PCB/kg KG.", which Bing Translator very respectably translates as " "The amount taken daily average currently by the adults of PCB (approx. 0.02 μg PCB/kg bw ) is well below the ATD of 1 μg PCB/kg. The breastfed infant, however, receives a significantly higher PCB intake (3 μg PCB/kg bw."
(12a) 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
(12b) Birnbaum and Slezak, Dietary Exposure to PCBs and Dioxins in Children, Environmental Health Perspectives * Volume 107, Number 1, January 1999, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566291/pdf/envhper00506-0029.pdf
(12c) Re: PCB levels in human milk: U.S. Agency for Toxic Substances and Disease Registry, Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000, at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf This ATSDR report quotes a range of concentrations of PCBs in human milk as from 238 to 271 ng/g lipid weight. 1 g lipid weight = about 25g whole weight (assuming 4% fat in human milk). So the concentrations found in the studies were about 250 ng/25g whole weight, which = 10ng/g whole weight. 1 g (gram) = 1 ml of water., so the 10 ng/g whole weight is the same as 10ng/ml. That is the same as 10,000 ng per liter, which is the same as .01 mg/liter. So the levels of PCBs in human milk seem to be about .01 mg/liter, compared with .0005 mg/liter, the maximum allowed by law in U.S. public water systems. That is, about 20 times the concentration that would be allowed in public water systems. (U.S.EPA, Drinking Water Contaminants, National Primary Drinking Water Regulations, at http://water.epa.gov/drink/contaminants/index.cfm#Organic)
(12d) Needham et al., Assessing Developmental Toxicant Exposures via Biomonitoring, Basic & Clinical Pharmacology & Toxicology Doi: 10.1111/j.1742-7843.2007.00185.x, p. 106 at http://onlinelibrary.wiley.com/doi/10.1111/j.1742-7843.2007.00185.x/epdf
(12e) Schell et al., Organochlorines, Lead, and Mercury in Akwesasne Mohawk Youth, Volume 111 | Number 7 | June 2003 • Environmental Health Perspectives, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241531/pdf/ehp0111-000954.pdf
(12f) 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. doi: 10.1289/ehp.1002134 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3094426/
(13). Jensen, A.A. et al, Chemical Contaminants in Human Milk, CRC Press, Inc., Boca Raton, Ann Arbor, Boston, 1991, p. 15. Findings of above confirmed in animal tests, with even greater contrasts, in Ahlborg et al., Risk Assessment of Polychlorinated Biphenyls (PCBs), Nordic Council of Ministers, Copenhagen. Report NORD 1992; 26
(14). 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 http://www.ncbi.nlm.nih.gov/pubmed/21237513
(15). Intake, fecal excretion, and body burden of polychlorinated dibenzo-p-dioxins and dibenzofurans in breast-fed and formula-fed infants. Abraham K, Knoll A, Ende M, Päpke O, Helge H. Children's Hospital, Virchow-Klinikum, Humboldt-Universität Berlin, Germany. at http://www.ncbi.nlm.nih.gov/pubmed/8910931 This study was cited in a 2002 EPA document ("Infant Exposure to Dioxin-like Compounds in Breast Milk") that apparently considered it to be fully valid.
(16). Infant Exposure to Dioxin-like Compounds in Breast Milk, Lorber and Phillips Volume 110 | Number 6 | June 2002 • Environmental Health Perspectives http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240886/pdf/ehp0110-a00325.pdf Also EPA Home/Research/Environmental Assessment: An Evaluation of Infant Exposure to Dioxin-Like Compounds in Breast Milk, Matthew Lorber (National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency) et al.
See also Improving the Risk Assessment of Persistent, Bioaccumulative, and Toxic Chemicals in Breast Milk, Workshop Summary Report, 2013, prepared for U.S. EPA by ICF International, at http://cfpub.epa.gov/ncea/risk/recordisplay.cfm?deid=262210: “… human infant blood levels of PBT (persistent, bioaccumulative and toxic) chemicals are 4-5 times higher than maternal blood levels at the end of a 4-month breastfeeding period.”
(16a) Weisglas-Kuperus N, Patandin S, Berbers GAM, Sas TCJ, Mulder PGH, Sauer PJJ and Hooijkaas H (2000). Immunological effects of background exposure to polychlorinated biphenyls and dioxins in Dutch preschool children. Environ. Health Perspect. 108: 1203-1207. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240203/
(16b) U.S. EPA: The Effects of Great Lakes Contaminants on Human Health at http://www.epa.gov/greatlakes/health/report.htm
(17b) Solomon et al., Chemical Contaminants in Breast Milk: Time Trends and Regional Variability, Environmental Health Perspectives • Volume 110 | Number 6 | June 2002Solomon et al., at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240888/pdf/ehp0110-a00339.pdf
(17b1) Verner et al., Measured Prenatal and Estimated Postnatal Levels of Polychlorinated Biphenyls (PCBs) and ADHD-Related Behaviors in 8-Year-Old Children, Environmental Health Perspectives, 2015, http://dx.doi.org/10.1289/ehp.1408084, at http://ehp.niehs.nih.gov/wp-content/uploads/advpub/2015/3/ehp.1408084.acco.pdf
(17d) WHO Regional Office for Europe, Air Quality Guidelines, Second Ed., 2000: Ch. 5.10: PCBs, p. 15,
(17e) Patandin, Effects of Environmental Exposure to Polychlorinated Biphenyls and Dioxins on Growth and Development in Young Children, 1999, Thesis, at Repub.Eur.Nl/Pub/19721/990106_Patandin,%20svati.Pdf
(18) RFD for PBDEs: EPA Technical Fact Sheet on Polybrominitated Diphenyl Eithers (PBDEs) and PBBs, p. 4 re RfD of 1 x 10-4 mg/kg/day (100 ng/kg-d) for BDE-47 and BDE 99 at www2.epa.gov/sites/production/files/2014-03/documents/ffrrofactsheet_contaminant_perchlorate_january2014_final_0.pdf
PBDEs, present in human milk in concentrations normally three times but up to 40 times the EPA’s RfD:
-Table 5-4 of EPA (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404, Schechter study in first page of table, showing 306 ng/kg-d as exposure for breastfed infants.
- Costa et al.,Developmental Neurotoxicity Of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Neurotoxicology. 2007 November; 28(6): 1047–1067. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052 Last paragraph of “Relevance to Humans” section, re up to 4.1 micrograms (4100 ng)/kg-day exposure of infants
18a) Regarding prevalence of tetraBDEs (BDE-47) compared with other forms of PBDEs, see Table 3-2 (p. 13) of U.S. EPA: Toxicological Review of 2,2',4,4'-Tetrabromodiphenyl Ether (BDE-47) EPA/635/R-07/005F www.epa.gov/iris. Accessed at http://www.epa.gov/iris/toxreviews/1010tr.pdf Also Costa LG, et al., Polybrominated diphenyl ether (PBDE) flame retardants: environmental contamination, human body burden and potential adverse health effects. Acta Biomed. 2008 Dec;79(3):172-83 at http://www.ncbi.nlm.nih.gov/pubmed/19260376. Petraes, in Envl Health Perspect, 7/2003, re “commonest” form.
(20). Developmental Neurotoxicity of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Costa et al., Neurotoxicology. 2007 November; 28(6): 1047–1067. doi: 10.1016/j.neuro.2007.08.007 PMCID: PMC2118052 NIHMSID: NIHMS34875 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052/
(22). Costa et al.,Developmental Neurotoxicity Of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Neurotoxicology. 2007 November; 28(6): 1047–1067. PMCID: PMC2118052 NIHMSID: NIHMS34875 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052/
(23). U.S. EPA (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. online at http://www.epa.gov/ncea or directly at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404
(24). Near end of Section 5.6.2 ("Impacts to Infants from Consumption of Breast Milk"), p. 5-79, of An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. online at http://www.epa.gov/ncea or directly at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404
(25). PBDEs in infant formula, detected at 32 and 25 pg/g wet weight: p. 4-77, 2nd paragraph of Section 4.7 (citing Schechter et al.) of U.S. EPA (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. online at http://www.epa.gov/ncea or directly at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404
PBDEs ingested by breastfed infants, 1,056 pg/g wet weight: Schecter et al., Polybrominated Diphenyl Ether (PBDE) Levels in an Expanded Market Basket Survey of U.S. Food and Estimated PBDE Dietary Intake by Age and Sex, Environ Health Perspect. Oct 2006; 114(10): 1515–1520, 4th paragraph from end, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1626425
(25a) Johnson-Restrepo, An assessment of sources and pathways of human exposure to polybrominated diphenyl ethers in the United States, Chemosphere. 2009 Jul;76(4):542-8. doi: 10.1016/j.chemosphere.2009.02.068. Epub 2009 Apr 5. at http://www.ncbi.nlm.nih.gov/pubmed/19349061
(27). Lien-Te Hsieh et al., Reduction of Toxic Pollutants Emitted from Heavy-duty Diesel Vehicles by Deploying Diesel Particulate Filters, Aerosol and Air Quality Research, 11: 709–715, 2011 ISSN: 1680-8584 print / 2071-1409 online doi: 10.4209/aaqr.2011.05.0058 at http://aaqr.org/VOL11_No6_November2011/8_AAQR-11-05-OA-0058_709-715.pdf
-- Also Wang et al., Emission estimation and congener-specific characterization of polybominated diphenyl ethers from various stationary and mobile sources, Environmental Pollution, Vol. 168, Oct. 2010
(28a) Quoted from Chen et al., Prenatal Polybrominated Diphenyl Ether Exposures and Neurodevelopment in U.S. Children through 5 Years of Age: The HOME Study , in Environmental Health Perspectives, May 2014, at http://ehp.niehs.nih.gov/wp-content/uploads/advpub/2014/5/ehp.1307562.pdf
29a) Eskenazi et al., In Utero and Childhood Polybrominated Diphenyl Ether (PBDE) Exposures and Neurodevelopment in the CHAMACOS Study Environ Health Perspect; DOI:10.1289/ehp.1205597 at http://ehp.niehs.nih.gov/wp-content/uploads/121/2/ehp.1205597.pdf
29b) Near end of Section 5.6.2 ("Impacts to Infants from Consumption of Breast Milk"), p. 5-79, of An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. online at http://www.epa.gov/ncea or directly at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404 “The average total concentration (sum of 13 congeners not including BDE 209) in the 4-year olds that had been breast fed (n = 202) was 3.6 ng/g lwt, compared to 1.3 ng/g lwt for formula fed (n = 44). “
(30). Roberts et al., Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ Health Study II Participants, published June, 2013 in Environmental Health Perspectives, at http://ehp.niehs.nih.gov/1206187/)
Chemosphere. 2006 Jun;64(1):79-85. Epub 2006 Jan 25 at http://www.ncbi.nlm.nih.gov/pubmed/16442149
(34). Exploration Of Perinatal Pharmacokinetic Issues Contract No. 68-C-99-238, Task Order No. 13 Prepared for: Office of Research and Development, U.S. Environmental Protection Agency Prepared by: Versar, Inc. EPA/630/R-01/004 Section 126.96.36.199, at http://www.epa.gov/raf/publications/pdfs/PPKFINAL.PDF
(35) Marques RC, et al., Hair mercury in breast-fed infants exposed to thimerosal-preserved vaccines. Eur J Pediatr. 2007 Sep;166(9):935-41. Epub 2007 Jan 20 This study found that mercury measured in infants’ hair increased 446% during the first six months of breastfeeding, while mercury measured in the mothers’ hair decreased 57%. These measurements included mercury from vaccines (still containing mercury at that time in Brazil, where the study was carried out), which the authors estimated accounted for about 40% of the infants’ exposure during those six months. Given that, combined with the finding in a Taiwanese study that over 95% of an infant’s exposure to mercury was from breastfeeding,(32) the increase in the infants’ mercury levels attributable to breastfeeding was probably well over 200% during the first 6 months of breastfeeding.
Also see footnotes 6, 15, 16, and 29 in D. Austin, An epidemiological analysis of the ‘autism as mercury poisoning’ hypothesis’, International Journal of Risk and Safety in Medicine, 20 (2008) 135-142 at http://researchbank.swinburne.edu.au/vital/access/manager/Repository/swin:9302
(36a) Oken et al., Maternal fish intake during pregnancy, blood mercury, and child cognition at age 3 years in a US cohort, Am J Epidemiol, May 2008 PMCID: PMC2590872 NIHMSID: NIHMS74985 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2590872.
Also Jedrychowski et al., Effects of prenatal exposure to mercury on cognitive and psychomotor function in one-year-old infants: epidemiologic cohort study in Poland, Ann Epidemiol, 2006 Jun;16(6):439-47. Epub 2005 Nov 7. at http://www.ncbi.nlm.nih.gov/pubmed/16275013.
Also Julvez et al., Sensitivity of Continuous Performance Test (CPT) at Age 14 Years to Developmental Methylmercury Exposure, Neurotoxicol Teratol. 2010 Nov–Dec; 32(6): 627–632. Published online Aug 10, 2010. doi: PMCID: PMC2980868 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2980868
(36b) Freire et al., Hair mercury levels, fish consumption, and cognitive development in preschool children from Granada, Spain, Environ Res. 2010 Jan;110(1):96-104. doi: 10.1016/j.envres.2009.10.005 at http://www.ncbi.nlm.nih.gov/pubmed/19909946
His HC et al.,The neurological effects of prenatal and postnatal mercury/methylmercury exposure on three-year-old children in Taiwan, Chemosphere. 2014 Apr;100:71-6. doi: 10.1016/j.chemosphere.2013.12.068. Epub 2014 Jan 23. at http://www.ncbi.nlm.nih.gov/pubmed/24461425
Cheuk et al., Attention-Deficit Hyperactivity Disorder and Blood Mercury Level: a Case-Control Study in Chinese Children Neuropediatrics 2006; 37: 234–240. at http://www.uni-kiel.de/medinfo/material/seminar_ws0809/Artikel%20Statistische%20Modelle%20WS%202008_09.pdf This study found over 9 times greater risk of ADHD among children with higher, but still relatively low, levels of methylmercury.
(37) . Attenuated growth of breast-fed children exposed to increased concentrations of methylmercury and polychlorinated biphenyls, P. Grandjean et al., FASEB J. (February 5, 2003) 10.1096/fj.02– 0661fje at http://www.fasebj.org/content/17/6/699.full.pdf
(39) Sokolowski et al., Methylmercury (MeHg) elicits mitochondrial-dependent apoptosis in developing hippocampus and acts at low exposures, Neurotoxicology 2011 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3256128/
(40) U.S. Agency for Toxic Substances and Disease Registry web page at http://www.atsdr.cdc.gov/training/toxmanual/modules/4/lecturenotes.html, saying "Methyl mercury is the most toxicological form of the element and, by its accumulation in the central nervous system (CNS), may result in neurotoxic effects…."
Also Berlin M. 1979. Mercury. Handbook on the Toxicology of Metals. Amsterdam: Elsevier.
(41) Burbacher et al., Comparison of Blood and Brain Mercury Levels in Infant Monkeys Exposed to Methylmercury or Vaccines Containing Thimerosal, (Oral Mg Kinetics section) Environ Health Perspect. 2005 August; 113(8): 1015–1021, PMCID: PMC1280342 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1280342
(41a) Gadad et al., Neuropathology and Animal Models of Autism: Genetic and Environmental Factors Autism Res Treat. 2013; 2013: 731935. Published online 2013 September 16. doi: 10.1155/2013/731935 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3787615/
Also Fenglian Xu et al., Mercury-induced toxicity of rat cortical neurons is mediated through N-methyl-D-Aspartate receptors Mol Brain. 2012; 5: 30. doi: 10.1186/1756-6606-5-30 PMCID: PMC3462706 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462706
(43). Bellés M et al., Behavioral effects and oxidative status in brain regions of adult rats exposed to BDE-99. Toxicol Lett. 2010 Apr 15;194(1-2):1-7. doi: 10.1016/j.toxlet.2010.01.010. Epub 2010 Jan 22. at http://www.ncbi.nlm.nih.gov/pubmed/20096757
(44). Gadad et al., Neuropathology and Animal Models of Autism: Genetic and Environmental Factors, Autism Res Treat. 2013; 2013: 731935 PMCID: PMC3787615 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3787615/
(45). Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models Deborah Rice et al., (of EPA's National Center for Environmental Assessment) at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1637807/
(47). Gary J. Myers et al., Postnatal Exposure to Methyl Mercury from Fish Consumption: a Review and New Data from the Seychelles Child Development Study, Neurotoxicology. 2009 May; 30(3): 338–349. Published online 2009 January 21. doi: 10.1016/j.neuro.2009.01.005 PMCID: PMC2743883 NIHMSID: NIHMS119840 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2743883/. Also see p. 518 of Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models, Deborah Rice et al., of EPA's National Center for Environmental Assessment, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1637807/
(47a) Yokoo et al., Low level methylmercury exposure affects neuropsychological function in adults, Environ Health. 2003; 2: 8. Published online Jun 4, 2003. doi: PMCID: PMC165591at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC165591
-- Lucchini et al., Neurotoxic effect of exposure to low doses of mercury, Med. Lav, 2002, at http://www.ncbi.nlm.nih.gov/pubmed/12197270
-- Carta et al., Sub-clinical neurobehavioral abnormalities associated with low level of mercury exposure through fish consumption, Neurotoxicology. 2003 Aug;24(4-5):617-23, at http://www.ncbi.nlm.nih.gov/pubmed/12900074
and in a dose-effect relationship:-- Carta et al., Neuroendocrine and neurobehavioral effects associated with exposure to low doses of mercury from habitual consumption of marine fish, Med Lav. 2002 May-Jun;93(3):215-24. at http://www.ncbi.nlm.nih.gov/pubmed/12197271
(50). Food Additives & Contaminants: Part B: Surveillance Volume 5, Issue 1, 2012 Robert W. Dabeka et al., Survey of total mercury in infant formulae and oral electrolytes sold in Canada DOI: 10.1080/19393210.2012.658087 at http://www.tandfonline.com/doi/full/10.1080/19393210.2012.658087#tabModule
(53) UN Environmental Programme: Chemicals: Mercury Programme Global Mercury Assessment, at http://www.chem.unep.ch/mercury/Report/Chapter3.htm
(57a) Hertz-Picciotto et al., Blood Mercury Concentrations in CHARGE Study Children with and without Autism, Environ Health Perspect. 2010 January; 118(1): 161–166.Published online 2009 October 19. doi: 10.1289/ehp.0900736 PMCID: PMC2831962
(57b) In two studies (published in 2007 and 2011), rats were exposed to methylmercury on postnatal day 7 (the neurodevelopmental equivalent of the time of birth in humans -- Clancy et al., Extrapolating brain development from experimental species to humans, Neurotoxicology (2007) at http://people.psych.cornell.edu/~blf2/pdfs/BCBLFNeurotox07.pdf ) in a single dose “that begins to approximate human exposure” (Sokolowski et al., Methylmercury (MeHg) elicits mitochondrial-dependent apoptosis in developing hippocampus and acts at low exposures, Neurotoxicology 2011 at www.ncbi.nlm.nih.gov/pmc/articles/PMC3256128) or in a dose “slightly higher than what is found in the general and primarily fish-eating human population that live on volcanic islands.” (Falluel-Morel et al., Developmental mercury exposure elicits acute hippocampal cell death, reductions in neurogenesis, and severe learning deficits during puberty, J Neurochem. 2007 December; 103(5): 1968–1981. author manuscript at www.ncbi.nlm.nih.gov/pmc/articles/PMC3363963) In both cases, the result was death of a significant number of brain cells; in the Falluel-Morel study, the hippocampus (important for brain function) was especially damaged. In that study, the juvenile rats were subjected to various tests, and the exposed rats did well in following cues but had “profound deficits” in learning ability, as found in two separate tests of memory.
(57c) Mahaffey et al., Blood Organic Mercury and Dietary Mercury Intake: National Health and Nutrition Examination Survey, 1999 and 2000, top lines of Tables 2 and 4, at www.ncbi.nlm.nih.gov/pmc/articles/PMC1241922/pdf/ehp0112-000562.pdf
Also, according to the Executive Summary of the NHANES survey, as provided by a CDC web page, “Total blood mercury levels are primarily composed of one type of mercury, methyl mercury, which enters the body mainly from dietary seafood sources.” http://www.cdc.gov/exposurereport/pdf/FourthReport_ExecutiveSummary.pdf
(57d) See also NRC (National Research Council)2000. Toxicological Effects of Methylmercury. Washington DC: National Academy Press.
(60a) Davidson et al., Mercury Exposure and Child Development Outcomes, at http://pediatrics.aappublications.org/content/113/Supplement_3/1023.full
(62). Laks DR, .Assessment of chronic mercury exposure within the U.S. population, National Health and Nutrition Examination Survey, 1999–2006.Biometals. 2009 Dec;22(6):1103-14. doi: 10.1007/s10534-009-9261-0. at http://www.ncbi.nlm.nih.gov/pubmed/19697139
(62a) National Scientific Council on the Developing Child, Early exposure to toxic substances damages brain architecture. (2006),Working Paper No. 4. at http://developingchild.harvard.edu/index.php/resources/reports_and_working_papers/working_papers/wp4/
(63). Autism rates associated with nutrition and the WIC program. Shamberger R.J., Phd, FACN, King James Medical Laboratory, Cleveland, OH J Am Coll Nutr. 2011 Oct;30(5):348-53. Abstract at www.ncbi.nlm.nih.gov/pubmed/22081621
(64). From Medscape Education Clinical Briefs "ACOG Issues Guidelines on Lead Testing in Pregnant and Breast-Feeding Women", Author: Laurie Barclay, MD CME Author: Désirée Lie, MD, MSEd CME/CE Released: 08/01/2012
(65a) U.S. FDA: Total Diet Study -- Market Baskets 2006-2011, at http://www.fda.gov/downloads/Food/FoodScienceResearch/TotalDietStudy/UCM184301.pdf
(66) Ettinger et al. (2014), Maternal Blood, Plasma, and Breast Milk Lead: Lactational Transfer and Contribution to Infant Exposure, Environ Health Perspect; DOI:10.1289/ehp.1307187 at http://ehp.niehs.nih.gov/1307187\
(66a1) Gundacker et al., Lead and mercury in breast milk, Pediatrics. 2002 Nov;110(5):873-8. at http://www.ncbi.nlm.nih.gov/pubmed/12415023
(66a2) Ettinger et al., Effect of breast milk lead on infant blood lead levels at 1 month of age, Environ Health Perspect. 2004 Oct; at http://www.ncbi.nlm.nih.gov/pubmed/15471729
(66a3) U.K. Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment: Survey of Metals in Infant Food. 2003/05, at http://cot.food.gov.uk/pdfs/TOX-2003-05.PDF, Table 2
(66a4) Dabeka, Survey of lead, cadmium, cobalt and nickel in infant formulas and evaporated milks and estimation of dietary intakes of the elements by infants 0-12 months old, Sci Total Environ. 1989 Dec 15;89(3):279-89.
(66a5) National Academy of Sciences, National Research Council, 1976: Recommendations for the Prevention of Lead Poisoning in Children, at https://books.google.com
(66a6) U.S. ATSDR, Lead, Ch. 6, at http://www.atsdr.cdc.gov/toxprofiles/tp13-c6.pdf, p. 372
(66b) U.S. Food and Drug Administration: Lipstick & Lead: Questions & Answers, at http://www.fda.gov/Cosmetics/ProductsIngredients/Products/ucm137224.htm#q2
(66c) Li et al., Transfer of lead via placenta and breast milk in human, Biomed Environ Sci. 2000 Jun, http://www.ncbi.nlm.nih.gov/pubmed/11055009
(66d) Ettinger et al., Effect of breast milk lead on infant blood lead levels at 1 month of age, Environ Health Perspect. 2004 Oct; at http://www.ncbi.nlm.nih.gov/pubmed/15471729
(66e) Dabeka, Survey of lead, cadmium, cobalt and nickel in infant formulas and evaporated milks and estimation of dietary intakes of the elements by infants 0-12 months old, Sci Total Environ. 1989 Dec 15;89(3):279-89.
(66f) Dabeka et al., Lead, cadmium and aluminum in Canadian infant formulae, oral electrolytes and glucose solutions, Food Addit Contam Part A Chem Anal Control Expo Risk Assess. Jun 2011; 28(6): 744–753.
(66g) Winiarska-Mieczan, Cadmium, Lead, Copper and Zinc in Breast Milk in Poland, Biol Trace Elem Res. 2014; 157(1): 36–44. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3895183/ Table 6
(66h) Bellinger, Very low lead exposures and children's neurodevelopment, Curr Opin Pediatr. 2008 Apr;20(2):172-7. doi: 10.1097/MOP.0b013e3282f4f97b.
(66j) Castellino et al., Inorganic Lead Exposure and Intoxications, CRC Press, 1995, at https://books.google.com; p. 141
(67) Needleman HL, Gunnoe C, Leviton A, et al. Deficits in psychologic and classroom performance of children with elevated dentine lead levels. N Engl J Med. 1979;300:689–695
-- also Bellinger DC, Stiles KM, Needleman HL. Low-level lead exposure, intelligence and academic achievement. Pediatrics. 1992;90:855–861
-- also McMichael AJ, Baghurst PJ, Wigg MR, Vimpani GV, Robertson EF, Roberts RJ. Port Pirie cohort study: environmental exposure to lead and children’s abilities at the age of four years. N Engl J Med. 1988;319: 468–475
(68) Kirk et al., Perchlorate and iodide in dairy and breast milk. Environ Sci Technol. 2005 Apr 1;39(7):2011-7. at http://www.ncbi.nlm.nih.gov/pubmed/15871231
-- Valentín-Blasini et al., Perchlorate exposure and dose estimates in infants, Environ Sci Technol. Published online Mar 30, 2011 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3084336/
(68a) Katharina M. Main et al., Human Breast Milk Contamination with Phthalates and Alterations of Endogenous Reproductive Hormones in Infants Three Months of Age, Environ Health Perspect. 2006 February; 114(2): 270–276. Published online 2005 September 7. doi: 10.1289/ehp.8075 PMCID: PMC1367843 at http://www.ncbi.nlm.nih.gov/pubmed/16451866
(68a1) web page of Medical Xpress 2011-2013, Science X network at http://medicalxpress.com/news/2012-04-breast-fed-infants-metabolize-perchlorate.html April 30, 2012
(68a2) Meeker, Exposure to Environmental Endocrine Disruptors and Child Development JAMA Pediatrics, Oct 2012, Vol 166, No. 10 at http://archpedi.jamanetwork.com/article.aspx?articleid=1171946 “Several phthalates are antiandrogenic… In human studies of adults, phthalates have been related to decreases in sex steroid and thyroid hormone levels, poor sperm quality….”
(68a3) Judy L. Cameron, Dept. of Psychiatry, Neuroscience, and Cell Biology and Physiology, University of Pittsburgh, in "Effects of Sex Hormones on Brain Development," Chapter 5 of Handbook of Developmental Cognitive Neuroscience, MIT Press, 200, edited by Charles A. Nelson and Monica Luciana.
(68b) Mortensen GK, et al., “Determination of phthalate monoesters in human milk, consumer milk, and infant formula by tandem mass spectrometry (LC-MS-MS),” Anal Bioanal Chem, 382(4):1084-92, 2005. at http://link.springer.com/article/10.1007%2Fs00216-005-3218-0
(68b1) Fredericksen et al., A Longitudinal Study of Urinary Phthalate Excretion in 58 Full-Term and 67 Preterm Infants from Birth through 14 Months, Environmental Health Perspectives, May 2014, at http://ehp.niehs.nih.gov/wp-content/uploads/advpub/2014/5/ehp.1307569.pdf, on p. 5:
(68c) Kim BN et al., Phthalates exposure and attention-deficit/hyperactivity disorder in school-age children. Biol Psychiatry. 2009 Nov 15;66(10):958-63. doi: 10.1016/j.biopsych.2009.07.034. Epub 2009 Sep 12. at http://www.ncbi.nlm.nih.gov/pubmed/19748073
See also Cho SC et al., Relationship between environmental phthalate exposure and the intelligence of school-age children.Environ Health Perspect. 2010 Jul;118(7):1027-32. doi: 10.1289/ehp.0901376. Epub 2010 Mar 1. at http://www.ncbi.nlm.nih.gov/pubmed/20194078
(68d) Meeker et al., Phthalates and other additives in plastics: human exposure and associated health outcomes. Philos Trans R Soc Lond B Biol Sci. 2009 Jul 27;364(1526):2097–2113.
Also Meeker et al., Human Exposure and Related Health Effects. In: Schecter A, editor. Dioxins and Health, 3rd Edition. Hoboken, NJ: John Wiley & Sons; 2012.
(68e) Main et al., Human Breast Milk Contamination with Phthalates and Alterations of Endogenous Reproductive Hormones in Infants Three Months of Age, Environ Health Perspect. 2006 February; 114(2): 270–276. doi: 10.1289/ehp.8075 PMCID: PMC1367843 at http://www.ncbi.nlm.nih.gov/pubmed/16451866
(68f) Associations of phthalates in school children with ADD and learning disability have also been found. (Chopra et al., Association between phthalates and attention deficit disorder and learning disability in U.S. children, 6-15 years Environ Res. 2014 Jan;128:64-9. doi: 10.1016/j.envres.2013.10.004. Epub 2013 Nov 19)
(70). Mondal et al., Breastfeeding: A Potential Excretion Route for Mothers and Implications for Infant Exposure to Perfluoroalkyl Acids, Environmental Health Perspectives http://dx.doi.org/10.1289/ehp.1306613 at http://ehp.niehs.nih.gov/wp-content/uploads/121/11/ehp.1306613.pdf
(70a) Adamović et al., Some observations concerning the ratio of the intake of organochlorine insecticides through food and amounts excreted in the milk of breast-feeding mothers, Bull. Environm. Contam. Toxicol. 20, 280-285 (1978), http://link.springer.com/article/10.1007%2FBF01683521?LI=true#page-1
(70b) Eckenhausen et al., Organochlorine Pesticide Concentrations in Perinatal Samples from Mothers and Babies, Archives of Environmental Health: An International Journal, Vol. 36, Issue 2, 1981, at http://www.tandfonline.com/doi/abs/10.1080/00039896.1981.10667611#.VOEi7S5mpME
(70c) Pesticides in the Diets of Infants and Children, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C. 1993, p. 232
(70d) USDA, Pesticide Data Program, Annual Summary, 2013, at http://www.ams.usda.gov/AMSv1.0/getfile?dDocName=STELPRDC5110007
(70e) Gebremichael et al., Analysis of organochlorine pesticide residues in human and cow's milk in the towns of Asendabo, Serbo and Jimma in South-Western Ethiopia, Chemosphere, 2013 Feb;90(5):1652-7. doi: 10.1016/j.chemosphere.2012.09.008. Epub 2012 Oct 11. at http://www.ncbi.nlm.nih.gov/pubmed/23062941
(70f) Subramaniam et al., Organochlorine pesticides BHC and DDE in human blood in and around Madurai, India, Indian J Clin Biochem. 2006 Sep; 21(2): 169–172. PMCID: PMC3454007 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3454007/
(70g) Fletcher et al., Serum levels of perfluoroalkyl acids in mothers and infants: transplacental and lactational transfer from the mother, Conference on Environment and Health Basel 2013, at http://www.iseepi.org/Conferences/Docs/2013_Basel_Abstracts.pdf
(71) La Leche League web page, “Pesticides and Breastfeeding” at http://www.llli.org/llleaderweb/lv/lvmayjun94p37.html
(72) R M Tripathi et al., Daily intake of heavy metals by infants through milk and milk products. Environmental Assessment Division, Bhabha Atomic Research Centre, Trombay, Mumbai, India. Science of The Total Environment (Impact Factor: 3.26). 04/1999; 227(2-3):229-35. DOI:10.1016/S0048-9697(99)00018-2 at http://www.ncbi.nlm.nih.gov/pubmed/10231985
(72a) Dabeka et al., Lead, cadmium and aluminum in Canadian infant formulae, oral electrolytes and glucose solutions Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2011 June; 28(6): 744–753. Published online 2011 May 31. doi: 10.1080/19393210.2011.571795 PMCID: PMC3118527
(72b) at http://pediatrics.aappublications.org/content/97/3/413.abstract
(72b1) Jackson et al., Arsenic concentration and speciation in infant formulas and first foods, Pure Appl Chem. 2012; 84(2): 215–223. Published online 2012 Jan 16. doi: 10.1351/PAC-CON-11-09-17 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3371583/ The study referred also to data from Ljung K, Palm B, Grander M, Vahter M. Food Chem. 2011;127:943.
72b2) Davidsson et al., Manganese absorption from human milk, cow's milk, and infant formulas
in humans, Am J Dis Child. <#> 1989 Jul;143(7):823-7 at https://www.ncbi.nlm.nih.gov/pubmed/2741855
72b3) Arora et al., Fetal and postnatal metal dysregulation in autism, Nature Communications, Article number: 15493 (2017) at https://www.nature.com/articles/ncomms15493
(72c) at http://www.atsdr.cdc.gov/toxfaqs/TF.asp?id=190&tid=34
(72c1) Kundakovic et al., Epigenetic perspective on the developmental effects of bisphenol A, Brain, Behavior, and Immunity (2011),doi:10.1016/j.bbi.2011.02.005, at http://champagnelab.psych.columbia.edu/docs/marija13.pdf
(72d) Sun et al. (2004), Determination of bisphenol A in human breast milk by HPLC with column-switching and ﬂuorescence detection. Biomed. Chromatogr., 18: 501–507. doi: 10.1002/bmc.345 at http://www.ncbi.nlm.nih.gov/pubmed/15386523
(72e) Yi et al., Association between Endocrine Disrupting Phenols in Colostrums and Maternal and Infant Health, Int J Endocrinol. 2013; 2013: 282381. Published online 2013 May 8. doi: 10.1155/2013/282381PMCID: PMC3662185 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3662185
(72f) Health Canada, Archived, Survey of Bisphenol A in Canned liquid Infant Formula Products, archived on June 24 2013. at http://www.hc-sc.gc.ca/fn-an/securit/packag-emball/bpa/bpa_survey-enquete-eng.php#fn2
(72g) “All infant formulae and foods tested for Bisphenol A (BPA) found free from BPA and safe for human consumption,” May 21, 2013, Ottawa, at http://www.inspection.gc.ca/about-the-cfia/newsroom/news-releases/2013-05-21/eng/1369152187993/1369152195012
(74). Hg Geier DA, A comprehensive review of mercury provoked autism Indian J Med Res. 2008 Oct;128(4):383-411, found at http://www.ncbi.nlm.nih.gov/pubmed/19106436
(74a) Exposure of young infants to environmental tobacco smoke: breast-feeding among smoking mothers. Mascola,et al., Am J Public Health. 1998 June; 88(6): 893–896. PMCID: PMC1508233 found at www.ncbi.nlm.nih.gov/pmc/articles/PMC1508233
(74b) at http://pediatrics.aappublications.org/content/108/3/776.full.pdf+html
(74d) ICF International, Workshop Summary Report, "Improving the Risk Assessment of Persistent, Bioaccumulative, and Toxic Chemicals in Breast Milk,” 2013, prepared for U.S. EPA, at http://cfpub.epa.gov/ncea/risk/recordisplay.cfm?deid=262210 p. b-80
(75). Mendola P et al, Environmental factors associated with a spectrum of neurodevelopmental deficits, Ment Retard Dev Disabil Res Rev. 2002;8(3):188-97 at http://www.ncbi.nlm.nih.gov/pubmed/12216063
(76). Dorman et al., Methods to Identify and Characterize Developmental Neurotoxicity for Human
Health Risk Assessment. III: Pharmacokinetic and Pharmacodynamic Considerations Environmental Health Perspectives • VOLUME 109 | SUPPLEMENT 1 | March 2001 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240547/pdf/ehp109s-000101.pdf
(77). Philippe Grandjean, in “Neurodevelopmental Disorders” in Children’s Health and Environment: A Review of Evidence, published by WHO, Regional Office for Europe, at http://www.euro.who.int/__data/assets/pdf_file/0007/98251/E75518.pdf p. 67
(78). Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. Lancet. 2006;368:2167–2178. at http://www.reach-compliance.eu/english/documents/studies/neurotoxity/PGrandjean-PjLandrigan.pdf p. 2
(78a) Winneke G. et al., Developmental aspects of environmental neurotoxicology: lessons from lead and polychlorinated biphenyls. J Neurol Sci. 2011 Sep 15;308(1-2):9-15. doi: 10.1016/j.jns.2011.05.020. Epub 2011 Jun 15.)
(78b) Kreuzer PE et al., 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and congeners in infants. A toxicokinetic model of human lifetime body burden by TCDD with special emphasis on its uptake by nutrition. Arch Toxicol
71(6):383–400 (1997). Also
LaKind JS et al., Methodology for characterizing distributions of incremental
body burdens of 2,3,7,8-TCDD and DDE from breast milk in North American nursing infants. J Toxicol Environ Health 59:605–639 (2000).
(79). 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
(80). S Patandin et al., Effects Of Environmental Exposure To Polychlorinated Biphenyls And Dioxins On Growth And Development In Young Children: A Prospective Follow-Up Study Of Breast-Fed And Formula-Fed Infants From Birth Until 42 Months Of Age Table 7.5 and accompanying text. at http://Repub.Eur.Nl/Res/Pub/19721
(81). Jens Walkowiak et al., Environmental exposure to polychlorinated biphenyls and quality of the home environment: effects on psychodevelopment in early childhood. Lancet 2001: 358: 1602-07 Abstract at http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(01)06654-5/abstract
(82). Schantz et al., Effects of PCB Exposure on Neuropsychological Function in Children Environmental Health Perspectives, Vol. 111 at at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241394/pdf/ehp0111-000357.pdf p. 363
(83) Jacobson et al., Effects of exposure to PCBs and related compounds on growth and activity in children Elsevier at http://www.sciencedirect.com/science/article/pii/089203629090050M
(83a) As reported by Rice (p. 57) in Bellinger, Editor, Human Developmental Neurotoxicology, Taylor and Francis, 2006,
HC et al.,The neurological effects of prenatal and postnatal mercury/methylmercury exposure on three-year-old children in Taiwan, Chemosphere. 2014 Apr;100:71-6. doi: 10.1016/j.chemosphere.2013.12.068. Epub 2014 Jan 23. at http://www.ncbi.nlm.nih.gov/pubmed/24461425
(84). Ilbäck NG et al., Methyl mercury exposure via placenta and milk impairs natural killer (NK) cell function in newborn rats. Toxicol Lett. 1991 Oct;58(2):149-58. at http://www.ncbi.nlm.nih.gov/pubmed/1949074
(85). Jusko et al., Pre- and Postnatal Polychlorinated Biphenyl Concentrations and Longitudinal Measures of Thymus Volume in Infants Environ Health Perspect. 2012 April; 120(4): 595–600. PMCID: PMC3339462. doi: 10.1289/ehp.1104229 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3339462/
(85a) Main KM, Kiviranta H, Virtanen HE, et al. Flame retardants in placenta and breast milk and cryptorchidism in newborn boys. Environ Health Perspect. 2007 Oct;115(10):1519–1526.
(86). Maternal asthma status alters relation of infant feeding to asthma in childhood.
Wright AL et al., Adv Exp Med Biol. 2000;478:131-7. Found at http://www.ncbi.nlm.nih.gov/pubmed/11065066
(87). Philippe Grandjean et al., Allergy and Sensitization during Childhood Associated with Prenatal and Lactational Exposure to Marine Pollutants Environ Health Perspect. 2010 October; 118(10): 1429–1433. PMCID: PMC2957924 found at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2957924
(88). Gene polymorphisms, breast-feeding, and development of food sensitization in early childhood. Hong X, J et al., Allergy Clin Immunol. 2011 Aug;128(2):374-81.e2. doi: 10.1016/j.jaci.2011.05.007. Found at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3149737/
(89). Infant feeding practices and physician diagnosed atopic dermatitis: a prospective cohort study in Taiwan. Chuang CH et al., Pediatr Allergy Immunol. 2011 Feb;22(1 Pt 1):43-9. doi: 10.1111/j.1399-3038.2010.01007.x. Found http://www.ncbi.nlm.nih.gov/pubmed/20573037
(90). Risk factors for atopic dermatitis in New Zealand children at 3.5 years of age. Purvis DJ, et al., Br J Dermatol. 2005 Apr;152(4):742-9. http://www.ncbi.nlm.nih.gov/pubmed/15840107
(91). Infant Feeding Practices and Nut Allergy over Time in Australian School Entrant Children, Jessica Paton, et al., Int J Pediatr. 2012; 2012: 675724. Published online 2012 July 3. doi: 10.1155/2012/675724 PMCID: PMC3397206 found at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3397206/
(92). Breastfeeding duration is a risk factor for atopic eczema. Bergmann RL et al., Clin Exp Allergy. 2002 Feb;32(2):205-9. Found at http://www.ncbi.nlm.nih.gov/pubmed/11929483
(93). Autism rates associated with nutrition and the WIC program. Shamberger RJ., King James Medical Laboratory, Cleveland, Ohio J Am Coll Nutr. 2011 Oct;30(5):348-53. At http://www.ncbi.nlm.nih.gov/pubmed/22081621
(94) Gascon, et al., Polybrominated Diphenyl Ethers (PBDEs) in Breast Milk and Neuropsychological Development in Infants, Environ Health Perspect; DOI:10.1289/ehp.1205266 at http://ehp.niehs.nih.gov/1205266/
(95) Hoffman, et al., Lactational Exposure to Polybrominated Diphenyl Ethers and Its Relation to Social and Emotional Development among Toddlers Environ Health Perspect. 10/2012; www.ncbi.nlm.nih.gov/pmc/articles/PMC3491946/ , seeing text above Figure 2.
(96). Rice DC, Effects of postnatal exposure of monkeys to a PCB mixture on spatial discrimination reversal and DRL performance. Neurotoxicol Teratol. 1998 Jul-Aug;20(4):391-400 at http://www.feingold.org/Research/PDFstudies/Rice98.pdf
(97). Driscoll LL et al., Chronic postnatal DE-71 exposure: effects on learning, attention and thyroxine levels. Neurotoxicol Teratol. 2009 Mar-Apr;31(2):76-84. doi: 10.1016/j.ntt.2008.11.003. Epub 2008 Nov 24. at http://www.ncbi.nlm.nih.gov/pubmed/19068229
(97a) IRIS document on Methylmercury, at http://www.epa.gov/iris/subst/0073.htm
(98) 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/full/pr20111086a.html¬
(99) Schantz et al., Effects of PCB Exposure on Neuropsychological Function in Children Environmental Health Perspectives, Vol. 111 at at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241394/pdf/ehp0111-000357.pdf p. 363
(81u) Oxford Journals Medicine Brain Volume 129, Issue 2 Pp. 290-292. Brainbrain.oxfordjournals.org Brain (February 2006) 129 (2): 290-292. doi: 10.1093/brain/awh729 Cognition, emotion and the cerebellum Jeremy D. Schmahmann et al.(81t7) http://water.epa.gov/scitech/swguidance/standards/criteria/aqlife/methylmercury/upload/2009_01_15_criteria_methylmercury_mercury-criterion.pdf Currently, U.S. EPA uses a RfD of 0.1 µg/kg body weight/day as an exposure without recognized adverse effects. (81y) quoted from EPA web page at http://www.epa.gov/hg/exposure.htm (84) In Prioritization of Toxic Air Contaminants - Children’s Environmental Health Protection Act, October, 2001: Dioxins
* About Pollution Action: Please go to www.pollutionaction.org
Some of many sources of exposure to mercury, other than consumption of fish/seafood and dental amalgam
“Mercury has been detected in blood, urine, human milk, and hair in individuals in the general population. Inhalation of mercury vapor in workplace atmospheres is the main route of occupational exposure to the compound. The most recent estimate (1983–1986) indicates that about 152,000 people, including over 50,000 women, are potentially exposed to mercury in workplace environments in the United States (RTECS 1998). Occupational exposure to mercury is highest in industries processing or using the element (e.g., chloralkali workers and individuals involved in the manufacturing of industrial instruments, thermometers, and fluorescent lights). Dentists and dental staff, house painters, chemists involved in the synthesis or analysis of environmental samples containing mercury, and individuals involved in disposal or recycling of mercury-contaminated wastes are also at risk of exposure.
“Members of the general public with potentially high exposures include individuals who live in proximity to former mercury mining or production sites, secondary production (recycling) facilities, municipal or medical incinerators, or coal-fired power plants. Other populations at risk of exposure include recreational and subsistence fishers who routinely consume meals of fish that may be contaminated; subsistence hunters who routinely consume the meat and organ tissues of marine mammals or other feral wildlife species; individuals with a large number of dental amalgams; pregnant women and nursing mothers (including their developing fetuses and breast-fed infants) who are exposed to mercury from dietary, medical, or occupational sources, or from mercury spills; individuals who use consumer products containing mercury (e.g., traditional or herbal remedies, or cosmetics, including skin lightening creams); and individuals living or working in buildings where mercury-containing latex paints were used, or where intentional (religious or ethnic use) or unintentional mercury spills have occurred.
“Mercury (elemental) has been identified in 714 of the 1,467 hazardous waste sites on the NPL.” (It should be noted that any waste site would contain broken fluorescent tubes, thermometers, electrical switches, etc. that would in many cases be leaking mercury.) Also later, from p. 453 of the same ATSDR document: “Commercial artists and crafts people are another group that is also at risk of mercury exposure from a variety of professional arts and crafts materials and techniques (Grabo 1997). This author reported that mercury was a hazard to commercial artists using mercury-based pigments in airbrush painting, brush paintings, and in pastels via pigment in chalk dusts. The author concluded that occupational health professions should be aware of toxic nature of the materials used by artists, whether they are employed in industry, self-employed, or are hobbyists. Chemists are another group at risk of occupational exposure as a result of activities involving the synthesis of mercury compounds or the analysis of environmental or biological samples containing mercury residues. Methylmercury compounds are still used in laboratory-based research, and so the possibility of occupational exposure remains. (above several paragraphs from Ch. 5. POTENTIAL FOR HUMAN EXPOSURE in ATSDR mercury profile at http://www.atsdr.cdc.gov/toxprofiles/tp46-c5.pdf)
Dioxins in formula less than 1% of dioxins in breast milk:
- Re dioxins in breast milk, at 242 pg TEQ, see footnote 5 above.
- Re dioxins in formula: U.K. Food Standards Agency Food Survey Information Sheet 49/04 MARCH 2004, Dioxins and Dioxin-Like PCBs in Infant Formulae, found at http://www.food.gov.uk/multimedia/pdfs/fsis4904dioxinsinfantformula.pdf According to their “upper bound” determinations (which they said were probably higher than actual concentrations) for 2003, almost all samples provided doses of 1.1 pg TEQ/kg body weight per day or less. Very compatible figures were found in the following: Weijs PJ, et al., Dioxin and dioxin-like PCB exposure of non-breastfed Dutch infants. Chemosphere. 2006 Aug;64(9):1521-5. Epub 2006 Jan 25 at www.ncbi.nlm.nih.gov/pubmed/16442144
PBDEs in formula less than 3% of concentration in breast milk:
- Re PBDEs in breast milk, 1,056 pg/g wet weight: Schecter et al., Polybrominated Diphenyl Ether (PBDE) Levels in an Expanded Market Basket Survey of U.S. Food and Estimated PBDE Dietary Intake by Age and Sex, Environ Health Perspect. Oct 2006; 114(10): 1515–1520, 4th paragraph from end, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1626425 This study was cited in the EPA document below, Section 5.6.2, 2nd paragraph.
- PBDEs in formula: Section 4.7 , p. 4-77, 2nd paragraph (citing Schechter et al., finding of 25 and 32 pg/g wwt, ) of U.S. EPA (2010) An exposure assessment of polybrominated diphenyl ethers. http:/cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404
Mercury in formula less than 1% as high as in human milk:
- See footnote 49 above re mercury in breast milk, at 8 ppb.
- Re mercury in infant formula at .03 ppb, see Food Additives & Contaminants: Part B: Surveillance Volume 5, Issue 1, 2012 Robert W. Dabeka et al., Survey of total mercury in infant formulae and oral electrolytes sold in Canada DOI: 10.1080/19393210.2012.658087 at
Re: PCBs in infant formula typically less than 1% but up to about 4% as high as in human milk:
- In breast milk: About 250 ng/g lipid weight. In soy-based formula: about 10 ng/g lipid weight. U.S. Agency for Toxic Substances and Disease Registry, Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000, pp. 560, 573, at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf Data does not appear to be available for PCBs in cow’s-milk-based infant formula, but data for whole milk could give an approximation, as follows: adding together the figures for the two kinds of PCBs in this study provides a range of 52 to 2455 ng/kg fat, which equals .05 to 2.45 ng/g fat (lipid) (Krokos et al., Levels of selected ortho and non-ortho polychlorinated biphenyls in UK retail milk, Chemosphere. 1996 Feb;32(4):667-73. at www.ncbi.nlm.nih.gov/pubmed/8867147)
* About Pollution Action: Please go to www.pollutionaction.org