Breastfeeding and Cancer
Some environmental toxins become concentrated in fat and are excreted in breast milk. Therefore:
1) Breastfeeding might lead to reduced risk of cancer for the mother; but also,
2) those toxins are ingested by a baby during a period of its life that precedes especially high cancer incidence among children, as well as at a time when infant brains are rapidly developing and vulnerable to effects of these chemicals. There are close, detailed correlations between highs and lows in breastfeeding rates and highs and lows in childhood cancer rates (as well as autism prevalence) among nations, among U.S. states, and among demographic groups. And while overall cancer incidence in the general population has been declining in both the U.S. and Europe in recent decades, childhood cancer has been increasing in both regions while breastfeeding rates have also been increasing. (Details to follow)
Diesel emissions and dioxins are classified as known carcinogens, and PAHs and PCBs are considered to be probable carcinogens. There is ample evidence (and no apparent disagreement) that these chemicals are ingested in many-times greater quantities by breastfed infants than by formula-fed infants. Average daily exposure of a breastfed infant to dioxin toxicity over the period of a year, as estimated by the EPA, is over 80 times higher than the reasonably-safe upper threshold of dioxin exposure estimated by the EPA. (authoritative sources to be cited later) The EPA also estimates that the average dioxin toxicity exposure of an infant breastfed for one year is six times that of an infant that had been bottle fed.
In a Japanese study of breast cancer risk, the authors pointed out regarding certain widely-used pesticides, “Organochlorines (including dioxins), which are poorly metabolized, accumulate in the human body via food intake, leaving breastfeeding as the primary means of excretion.” (26) It is very possible that accomplishing that excretion is beneficial to a mother’s long-term health (although the above study of breast cancer risk did not find any such benefit). A U.S. study found especially high benefits accruing to a mother who breastfed twins for two years, finding a decrease of about 70% in the mother’s body burden of dioxins over the two-year period. (27) One study of dioxin concentrations in infants of various birth orders found that, the closer the infant had been to first in birth order, the higher the dioxin concentrations in the deceased infants’ tissues, “thus showing that the mothers can decontaminate themselves by breast feeding.” (27-0) The authors of the study, in conformity with conventional beliefs in the medical community, saw no problem with this. When a quantity of toxins that might be hazardous to a 120-pound person is excreted from her and completely ingested by a 7-pound infant, at an especially vulnerable time of the infant's development, it's obvious that doing this is a good idea for all concerned, isn't it?
Dioxins, in addition to being carcinogens, are also known to be neuro-developmental toxins. A U.S. study of all 50 U.S. states and 51 U.S. counties found "a direct correlation (of increased autism) with the increasing percentage of women exclusively breast-feeding."(27e)
Points such as the above have been brought up in letters to high officials of the American physicians' associations and of the U.S. Department of Health and Human Services, and none of them have responded with any criticism of those statements. They point to the "recognized" benefits of breastfeeding and the "risks" of not breastfeeding, as presented by U.S. Surgeon General Benjamin.(27f) However, looking at historical health data (from CDC, NIH and other authoritative sources) regarding the diseases and conditions referred to as risks of not breastfeeding, it turns out that there has been significant worsening in child health in all but one of those areas during the years of the transition from low rates of breastfeeding to high rates. And this has not merely been a general worsening over decades, while many toxins have been increasing in the environment. The specific times of the fairly abrupt increases of disorders for particular age groups correlated fairly precisely with the specific times of those age groups' earlier sharply increased exposures to breastfeeding. There were many cases in which
a) breastfeeding rates of particular ethnic, socio-economic and national groups were high or rapidly increasing while breastfeeding rates were low or not rapidly increasing for other populations, and (tracking in close correlation with the above)
b) the disease rates of those particular groups were high or rapidly increasing while disease rates of the other populations were low or not rapidly increasing.
In the cases of three of the disorders alleged to be reduced by breastfeeding, actual epidemic increases have been declared in those specific diseases or conditions, all of which major increases occurred following the transition to higher rates of breastfeeding. For details on all of the above, with citations from authoritative sources, go to www.breastfeedingprosandcons.info/ .
Childhood cancer and carcinogens in breast milk
Some of the toxins that are known to become concentrated in breast milk (see Section 2.2) are recognized causes of cancer. One of the forms of dioxins is classified by the International Agency for Cancer Research as a known carcinogen. (Note in Section 2.3 that dioxins are known to the EPA to typically be especially highly concentrated in breast milk.) PCBs, also known to be concentrated in breast milk (Section 2.2 ), are known to be carcinogens in animal tests and are considered, along with the other variations of dioxins, to be probable carcinogens for humans. Tobacco smoke products: 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."(27g) (Cotinine is a marker for smoke exposure) PAHs are known to cause cancer in animals; and they come from sources that are known human carcinogens (diesel emissions and tobacco smoke), both of which are known to contribute PAHs to breast milk. (See Section 3) Even though PAHs may be the only probable carcinogens from within diesel emissions and tobacco smoke that have been specifically measured in breast milk, it would be surprising if some of the various other toxic ingredients of both diesel emissions and tobacco smoke weren't also present in breast milk.
Even though only one major form of dioxins has been officially classified as a known carcinogen, the other variations of dioxins have been characterized by EPA as likely to be human carcinogens, which are "anticipated to increase the risk of cancer at background levels of exposure."(106a1)
NOTE the following:
(a) the average daily exposure to dioxin toxicity of an infant breastfed for one year, as estimated by the EPA, is 86 times the reasonably-safe upper threshold of dioxin exposure estimated by the EPA in 2012 (34c, 34b), and
(b) the accumulated dioxin toxic equivalency in infants breastfed for one year was found to be six times higher than that in bottle-fed infants, in an EPA study. (83)
With the above in mind, note the following:
1.1) According to a study by a medical researcher with the University of Mainz, Germany, “Incidence rates (of childhood cancer) range from 130 (British Isles) to 160 cases (Scandinavian countries) per million children.”(106b) Bear in mind that the countries of the British Isles (U.K. and Ireland) are at the low end of European rates of breastfeeding, and the Scandinavian countries (with their 23%-higher average cancer rate) are at the high end of breastfeeding rates. (see www.breastfeeding-and-cancer.info/breastfeeding-locations.htm ) Filling in with data about relevant developed countries that are missing from the above comparison, with information from the International Agency for Research on Cancer (IARC), childhood cancer incidence in low-breastfeeding France was higher than in the British Isles, but still substantially lower than the incidences in eight of the nine high-breastfeeding countries listed. (106b1) A British university study indicates that the final low-breastfeeding European country, Belgium, is also in the low childhood-cancer group; it also found that only one out of eight high-breastfeeding countries had a childhood cancer rate low enough to be within the range that included all of the low-breastfeeding countries, and that single rate was at the top end of the low-breastfeeding countries' range.(106d)
1.2) Major types of childhood cancers are known and/or suspected to be more common in families of higher socio-economic status(106c) and educational level. For central nervous system (CNS) tumours, the odds ratio for16 years of parental education was 1.69 (95% CI: 1.25–2.30) (roughly 69% greater likelihood) compared with parents who did not complete high school, in a major California study (von Behren et al.);(106c3) this apparently much greater prevalence of CNS cancer among children of highly-educated parents has been a source of puzzlement, since "Highly educated people are more likely to hold managerial and professional jobs, which usually have few known carcinogenic exposures." It is a recognized fact, but apparently not well known, that (a) college graduates are typically twice as likely to breastfeed as high school graduates, and (b) that breast milk contains many-times higher concentrations of carcinogens than alternative feedings. (see above and Section 2.4)
1.3) Ethnic differences: It has been well reported that childhood cancer rates are highest among whites, a little lower among Hispanics, and much lower among blacks.(106c1) In this regard, note that breastfeeding rates are highest among whites, a little lower among Hispanics, and about 50% lower among blacks. (see www.breastfeeding-and-cancer.info/breastfeeding-demographics.htm)
The white-black ratio of incidence is especially high (2.2 to 1) in infant cancer of the central nervous system;(106c1) this is as could be predicted from the fact that dioxins, which are known to be highly concentrated in breast milk (Section 2.2) are lipophilic: attracted to fat. Fat is the principal component of nerve tissue, which would therefore be the site to which the dioxins in breast milk would gravitate most, and where the dioxins' cancer-causing effects would be most significant.
1.4) Both older parental age and being first-born are linked with several childhood cancers.106c2 Older mothers are more likely to breastfeed, they are likely to breastfeed for longer periods, and their lifetime accumulated body burdens of persistent toxins will be higher than those of younger mothers. Firstborn babies are more likely to be breastfed, they are likely to be breastfed for longer periods, and the levels of carcinogens in earlier breast milk will be higher since the toxins will not have been excreted during earlier breastfeeding. (see www.breastfeeding-and-cancer.info/breastfeeding-demographics.htm)
In the dioxin-exposure chart (upper left), special attention should be given to the upper three lines, which indicate dioxin exposure via breastfeeding for 6 months or more. The full extent of the similarity between those lines and the lines in the cancer-incidence chart on the right might not be obvious at first glance, due to the deletion of empty space from the lower part of the right-hand chart. It should be noted that the percentage decline from maximum dioxin impact of breastfeeding (during infancy) to the minimum impact (at age 10) is about 60%, which corresponds closely with the percentage decline in childhood cancer from the early peak period to the low at age 10.
When observing the high levels of childhood cancer that occur in the first years after birth, it may seem unlikely that many of those could result from carcinogenic exposure after birth, if one thinks in terms of some well-known carcinogens that have very lengthy latent periods. But carcinogens and cancer types vary; also, "rapid cellular proliferation" is taking place while children's bodies are growing, which no doubt affects the speed of cancer growth. A tumor latency period in rats of four weeks after exposure to a carcinogen is apparently typical, and it is often less than three weeks in hamsters.(106c20)
The chart in the EPA-provided study, above left, shows "lipid concentrations" becoming nearly equal between formula-fed and breastfed infants after about 10 years; but it is also recognized that accumulated body burden of persistent toxins (such as dioxins) is important in assessing potential harm. Therefore that study's authors also provide data for the "AUC" (area under the curve) for the various feeding possibilities, showing far higher accumulations of dioxins still prevailing in breastfed children at age 10.
According to the CDC, "The cause of most childhood cancers is not known, although some of these cancers are the result of genetic predisposition (cancer runs in the family)." When looking at the childhood cancer incidence charts below, major changes in the long-term trend of U.S. childhood cancer incidence are conspicuous, which couldn't possibly have resulted from genetic changes so quickly. That means that there have probably been changes that have taken place in the environment. Bear in mind that (a) what infants are fed is very much a part of the environment, and (b) there have been major changes in infant feeding practices in recent decades, as shown below.
As indicated in the "National Trends in Breastfeeding Rates" chart (upper chart above), the paths of U.S. breastfeeding trends have been very uneven. The turns in these rates are worth observing in relation to changes that have taken place in childhood cancer rates in recent decades. Looking at the U.S. childhood cancer rates since 1975 (above), one can see some apparent similarities between changes in breastfeeding rates and changes in childhood cancer incidence, as follows:
1) The strong upward trend in breastfeeding rates up through 1983 is conspicuous, as is the upward slope in cancer rates through the late 1980's.
2) Observe the mild downturn in breastfeeding that began in 1983. Then note the leveling and mild downturn in childhood cancers that took place about seven years later.
3) Observe the distinct upturn in breastfeeding rates that began in 1991. Then note (in the Historical Trends 1990-2009 chart) the distinctly higher level in childhood cancers that began seven years later.
Examples above suggest a latency period of seven years for some of the carcinogens in breast milk. But there are many variations of dioxins, as well as other carcinogens present in breast milk (various forms of PAHs from tobacco smoke and diesel emissions, at minimum -- see Section 3); and there are a number of different kinds of cancer; and there are almost certainly different latency periods for various of the carcinogens (known or probable) present in breast milk.
As can be seen in this "Historical Trends (1975-2009)" chart, cancer trends in the general U.S. population were contrary to the downturn in childhood cancer after 1990 seen just above, and also contrary to the upturn in childhood cancer after 1997 seen above.
For all age groups, the decline in cancer rates after 1998 is as should have been expected following successful national efforts to reduce pollutants in the environment. Childhood cancer should have been expected also to have fallen in response to those same reductions, including reductions in the effects of sidestream smoke from parents and caregivers. But, instead, childhood cancer has been rising while cancer in the general population has been declining. That strongly implies the existence of a widespread, growing source of carcinogens to which children, specifically, are exposed. There is one (and probably only one) obvious candidate for being a widespread and growing source of carcinogens to which children, specifically, are exposed: Looking at the "National Trends in Breastfeeding Rates" in Figure 2 above, observe the increases in breastfeeding during the 1990's, and bear in mind (a) the extremely high concentration of dioxins in breast milk and (b) the many-times-higher concentration of dioxins in breast milk than in formula. (see NOTE in 3rd paragraph of this section)
Observations about childhood cancer rates cited above apply to the U.S., with strong ups and a mild extended downturn in childhood cancer that correlated well with the strong ups and a mild extended downturn in U.S. breastfeeding rates. On the basis of research into childhood cancer data for Europe, a thorough study published in 2004 referred to "clear evidence of an increase of cancer incidence in childhood and adolescence during past decades."(106c2a) In correlation with that, note that overall breastfeeding rates in Europe appear to have been generally upward in recent decades (see Figure 1.9), without a several-year general downturn such as occurred in the U.S. in the 1980's. And also as in the case of the U.S., the increasing childhood cancer in Europe continuing into the 2000's went counter to a downward trend in all-age cancer incidence in Europe during that same period; except for obesity-related cancers, cancer incidence in Northern and Western Europe declined after the mid-1990's.(106c2b) As in the U.S., the general decline in cancer rates was as expected, following successful efforts to reduce exposures to carcinogens.
So childhood cancer incidence has been
1) out of step with general cancer rates, in both the U.S. and Europe, and
2) in tandem with breastfeeding rates, in both continents.
The correlation of childhood cancer with breastfeeding should not be a surprise, given that breastfeeding subjects infants to very extended dioxin toxicity exposure at levels that the EPA considers to be over 80 times a safe daily dose, causing accumulated dioxin toxic equivalency in infants breastfed for one year that is six times higher than that in infants that had not been breastfed. And, given the close connection of much childhood cancer specifically with breastfeeding (more on this to follow), it is also not surprising that childhood cancer rates (rising) have been out of step with general cancer rates (falling).
1.7) Although the principal concerns being discussed here are childhood cancer rates and the major source of ingestion by infants of carcinogens, general cancer rates are also of relevance. Those general rates are good indicators of the variations in presence of carcinogenic toxins among different states, and concentrations of those toxins in local breast milk would also vary among different states. (But it should be kept in mind that levels of carcinogens in breast milk are affected not only by local area conditions but also by a mother's consumption of foods that are typically shipped in from distant locations, as well as by very individual factors such as tobacco smoke containing PAHs, air with dioxins from backyard burning or from local diesel traffic, residential wood-burning emissions, etc.)
a) industry-, traffic- and population-generated pollution of the Northeast and Midwest regions,
b) agricultural chemical pollution in major crop-growing states, and
c) other special aspects of the environment such as considerable shipping-related diesel emissions going deeply into populated areas in Louisiana (see the only orange-colored state on the south coast, with details in Section 3) or extraordinarily high dioxin emissions in Kentucky (see the only dark-red state outside the Northeast coastal corridor, with more information at www.breastfeeding-and-cancer.info/breastfeeding-locations.htm .
If one wants to find a part of the U.S. in which to look for effects of a previously little-explored source of carcinogens, without having the picture heavily clouded by presence of many other sources of carcinogens such as in the regions mentioned above, it appears (from the above map) that the western U.S. should be a useful place to look. One logical place to start is with the EPA's "Carcinogenic Risk" map, in this next map. As is apparent, this map is not good at predicting which states will be higher or lower in cancer incidence when comparing it with the "All Ages" cancer incidence rate map, above right. When comparing it to the childhood cancer incidence map, lower left, the comparison is better, but still not at all good. Notice how California's actual childhood cancer incidence is similar to that of Idaho, despite great contrasts in the two states' risk levels as determined by the EPA. And Utah, with its low level of carcinogens as perceived by the EPA, stands out like the proverbial sore thumb in its childhood cancer incidence.
A brief perusal of the EPA's website will reveal that a huge amount of research has gone into assessing carcinogenicities of various substances and determining their levels in the environment across the U.S. So it is disappointing to see this illustration of the EPA's below-par ability to find higher or lower carcinogenic risk in places that prove to actually have higher or lower childhood cancer rates.
There is an alternative method for assessing childhood cancer risk that is much better than that of the EPA. Look closely at this next chart (with cancer rates taken from the map above and breastfeeding data from the CDC), and think of what the odds are that something like this is a matter of chance, rather than a demonstration of cause and effect. It may be helpful to review the beginning of this section concerning the carcinogens known to be concentrated in breast milk, and also concerning the extremely high levels of carcinogens in breast milk in relation to the levels in alternative feedings.
As mentioned, the U.S. West is a good area in which to demonstrate the effects of one particular source of carcinogens, since it has much less of other sources of carcinogens as compared with the eastern and central U.S.; the greatly varying levels of the other sources of toxins in those other states greatly complicate the picture outside the West. However, even when looking closely at data for the eastern and central U.S. states, one can see that varying rates of breastfeeding are also fairly accurate at predicting levels of childhood cancer in those other states as well. That can be seen in Appendix B.
1.8) The Northeast Coast
The author of this paper has taken a look at comparative breastfeeding and childhood cancer data for only one other individual U.S. region: the highly-populated Northeast corner. That is another useful region in which to look for effects of an individual source of carcinogenic exposure of infants, since the pollution there is relatively uniform; pollution in that region is apparently related more to land traffic, coastal shipping, and prevailing winds that carry toxins long distances from the South up the coastal corridor, and less related to the highly variable local effects of heavy industries and agricultural chemicals that are typical in most other regions.
Looking at the states in this map other than Rhode Island, this could be a good illustration of the effects of air pollution in affecting childhood cancer rates. Vermont (VT) is low in density, traffic, industry, and pollution, and (not coincidentally) also unusually low in childhood cancer. But Rhode Island is right in the middle of the high-density, high-traffic coastal corridor, with as much pollution as in the surrounding, higher-cancer states. Yet it has markedly lower childhood cancer incidence. Could it have anything to do with the fact that Rhode Island's breastfeeding rates are well below the rates of every one of its neighbors in the region? (106c2c) It appears that this region's pollution, although significant, isn't toxic enough to cause seriously increased childhood cancer unless it becomes concentrated on its way to being ingested by infants. (See Section 2.3 about lactation's efficiency as a means of concentrating environmental chemicals into breast milk.)
One might also wonder whether it is surprising that New Hampshire and Massachusetts are
a) highest and second highest in breastfeeding rates in the region and are also
b) highest and tied for second highest in cancer incidence.
Maine is tied with Massachusetts in childhood cancer incidence despite being slightly lower in breastfeeding rates; but greater effects from the environment in Maine are to be expected, considering Maine's disadvantages related to lower levels of sunlight (resulting in elevated dioxin levels and other negative effects) and its citizens' relatively high average exposure to smoke from residential wood burning. (See www.breastfeeding-and-cancer.info/breastfeeding-locations.htm)
It is interesting to note that Vermont's breastfeeding rate is even higher than that of New Hampshire, yet its cancer rate is only medium. This verifies that the problem is not inherent in breast milk, the problem is that lactation is effective at taking in mild doses of toxins from the environment and then concentrating those toxins in breast milk. New Hampshire has a great deal of typical coastal-Northeast regional pollution that can be gathered into women's bodies and then concentrated in breast milk, but Vermont does not have such a level of pollution.
The reader is urged to take another thorough look at these last maps and charts, and think again about how likely it is that the correlations shown between higher or lower breastfeeding rates in various states and later higher or lower childhood cancer rates in those same states is a chance occurrence, rather than a demonstration of cause and effect. Mothers who live in medium- or high-pollution areas may do well to think about the above when deciding whether or not to breastfeed their infants.
There is still much more evidence linking childhood cancer incidence with breastfeeding, but enough has been said here for present purposes. Additional material on this subject will be found in the Appendix .
There is one known source of carcinogens that correlates well with childhood cancer in all of the respects below. Can you think of any other source of carcinogens that makes such a close fit with childhood cancer in even one respect, not to mention all nine?
1) Exposure of a large percentage of contemporary infants to the particular source of carcinogens is considered by the EPA to result in extended ingestion of a known or probable carcinogen at a rate scores to hundreds of times higher than the EPA's estimated safe level for that toxin; (see 3rd paragraph of Section 1, above)
2) infant exposure to the particular substance in question ranks by U.S. states from top to bottom in excellent correlation with childhood cancer rates in those same U.S. states several years later; (see the last two charts above and also Appendix B)
3) exposure to the source of carcinogens in question is highest in European countries that are highest in childhood cancer, and lowest in European countries that are lowest in childhood cancer; (see Section 1.1 above)
4) exposure to the particular substance in question is highest in the U.S. ethnic group that has the highest incidence of childhood cancer, and lowest (by a wide margin) in the ethnic group that has by far the lowest incidence of childhood cancer (see Section 1.3 above);
5) ingestion of the substance in question results in exposure by age of infant that tracks rather accurately ahead of cancer rates by age of infant (initially high, then rapidly declining -- see charts in Section 1.5);
6) ingestion of this substance in question results in exposure by birth order that correlates with higher childhood cancer rates by birth order; it is similar with parental age 1.4
7) exposure of U.S. infants to the known carcinogens in that substance over the last four decades went through major changes in levels, with times of multi-year general changes in exposure that correlate well with (and ahead of) multi-year changes in actual childhood cancer incidence (see second set of charts in this section);
8) in two out of three of the above-mentioned cases of changes, childhood cancer incidence increased while adult cancer rates declined; this means that the particular substance in question would be one to which children, specifically, have been increasingly exposed;
9) it is a widespread exposure that results in unusually high ingestion of carcinogens by those infants receiving it, according to an EPA study's estimates.(83)
If anyone can think of any other source of carcinogens that is shown by authoritative health data to be so closely linked with childhood cancer risk (or even remotely as closely linked), please e-mail to firstname.lastname@example.org.
There is an additional important characteristic of breastfeeding as a source of toxins known to lead to cancer: It is a major source of multiple carcinogens to infants that could be shut off almost overnight, if people were to just decide to do so. Long-term research studies are obviously desirable, and efforts to reduce toxins in the environment are obvious desirable, but in the meantime millions of children are continuing to ingest high doses of known carcinogens as a result of an exposure that doesn't really have known benefits that justify that known exposure. A close examination of the alleged benefits as laid out by Surgeon General Benjamin, looking at data showing what actually occurred in children's health data after the U.S. transition from low to high breastfeeding, shows that none of the benefits actually materialized as would have been projected. In fact, the health outcomes actually became significantly worse in all but one of the conditions that should have improved if there had been validity to the alleged benefits of breastfeeding. In three important areas, diabetes, obesity, and allergies (including asthma), the results were so much worse following the increases in breastfeeding that they were declared to be epidemics. (see www.breastfeedingprosandcons.info for details and sources regarding the above points)
As a far faster-acting alternative remedial measure (compared with long-term studies), there is something we could easily do now that would quickly and greatly reduce infants’ ingestions of all or almost all of these same strongly-suspected developmental toxins and known carcinogens. That measure would be as follows: to enable parents to make up their own minds about breastfeeding on the basis of at least moderately complete, non-misleading information about the matter. As of now, parents have been receiving essentially nothing but one-sided views on the subject of breastfeeding, including impressive-sounding figures about health benefits of breastfeeding without proper acknowledgment of the weakness of the evidence for those claims. These presentations are so distorted as to be basically inaccurate. Parents are told almost nothing about the well-recognized (but unpublicized) toxic exposures brought on by breastfeeding. A moderately valid presentation of the subject matter to parents would conspicuously make the point (acknowledged only inconspicuously by the Surgeon General) that there is no proof that bottle feeding leads to adverse health conditions in children in developed countries; and it would also present the points that, following the transition from a very low-breastfed generation of children to highly-breastfed generations, almost every one of the illnesses said to result from not breastfeeding actually increased, several of them very substantially. The only one that didn't increase at least did not decline, as should have been expected if there had been validity in the claims of benefits of breastfeeding. It should also be clarified to prospective nursing mothers that the possible health benefits to the mother are mainly achieved by excreting toxins out of the mother which are then ingested by the infant, during the most vulnerable period of the infant's life.
A question that should be addressed to those who are recommending breastfeeding, but which they probably won't want to answer:
Given (a) the inconclusiveness of the studies that support breastfeeding,** (b) the known concentrations of environmental toxins in recent human milk,** and (c) the many close correlations between variations in breastfeeding levels and similar variations in levels of several epidemics of childhood diseases (seen in national health data**): What assurance is there that breastfeeding is more beneficial than harmful?
** Supporting information and references to authoritative sources regarding matters raised in this question are included in a one-page printable version of this question, to be found at www.pollutionaction.org/Q.pdf .
We have good reason to say that those who recommend breastfeeding probably will not have an answer to the above question. A slightly different version of essentially this same question was mailed to four different high officials at the U.S. Department of Health and Human Services, who are heads of divisions that are involved in promoting breastfeeding. As of 7 and more weeks after mailing those letters, no reply has been received. Several months earlier, each of those officials had sent one response to an earlier letter that brought up the matters above, and none of their responses said anything in criticism of any of those points. Those points are all well substantiated. So the question that comes at the end, above, is a logical question to ask. But the promoters of breastfeeding appear to be unwilling or unable to respond to it. If they can't or won't answer that question as part of an informed debate on this matter (therefore to email@example.com, as well as to you), should anybody pay attention to their advice?
Specifics about certain carcinogens
Dioxins and certain PAHs (Polycyclic Aromatic Hydrocarbons) are categories of chemicals widely distributed in the environment that are known or likely carcinogens. One important form of dioxin is a known carcinogen, other forms of dioxins are classified as probable carcinogens, and PAHs are well known to cause cancer in animals.28a
Sources of these carcinogens: The EPA's web pages and documents on dioxins and PAHs point out major sources of dioxins and PAHs as follows: (a) dioxins are unintentional byproducts of several industrial chemical processes and of most forms of combustion, including fuel emissions, backyard burning, waste incineration, and wildfires, and are also found in weed killers used on agricultural lands; (b) PAH's are also unintentional products of typical forms of combustion, including cigarette smoking, residential wood burning and vehicle emissions.(34) The ATSDR and the EPA point out that dioxins are released by municipal solid waste and industrial incinerators, hospital waste incinerators, backyard burning, vehicle exhaust (mainly of diesel vehicles), emissions from oil- or coal-fired power plants, soil erosion and surface runoff. (Note that most of the above sources are related to population density and combustion processes.) Animal fat in the diet accounts for close to 90% of dioxin exposure in the United States, according to a 2003 National Academies of Science report on dioxins in the food supply. (34a) Vegetarians are reported to consume only 2 percent of the dioxin load of the general population, because their diet is dominated by foods low on the food chain. (34d) Parents should consider the above sources of carcinogens and think how much exposure women generally have to each of them as compared with the exposures cows have to these sources of environmental toxins.
The predominant source of high doses of these toxins to infants:
To provide an idea of how much dioxin is a significant hazard to human infants, note that (in its most recent dioxin assessment, issued February, 2012), the EPA set the threshold for safe dioxin exposure at a toxicity equivalence (TEQ) of 0.7 picograms per kilogram of body weight per day.(34b) Drawing on more recent research, that standard is somewhat stricter than the goal set earlier by the World Health Organization, of 1 pg TEQ/kg bw/day.”(36) With those estimates of safe dose in mind, note that what appears to be the only EPA estimate of infant exposure to dioxins predicts that an infant breastfed for one year would receive an average daily dose of about 60 pg of TEQ/kg bw/day.(34c) So the average daily dose of 60 pg, over the period of a full year of rapid development, is 86 times the estimated safe dioxin exposure of 0.7 pg. The above data are very compatible with findings in other studies, from various countries. (34e)
The above figures are estimated average daily exposures over a first year of breastfeeding, taking into account the lower levels that occur later in the year during the course of excretion by way of lactation. The peak body-weight-based dose received by a breastfeeding infant is estimated in an EPA study to be 242 pg TEQ/kg-day.(37a) Note that these extremely unsafe exposures of breastfed infants come shortly before a high-level period for development of childhood cancer.
Lactation as an effective means of taking in mild doses of toxins through being in developed areas in recent years, and then concentrating those toxins in breast milk:
Bearing in mind that PCBs are typically considered to be a form of dioxin, note the following: According to the U.S. Agency for Toxic Substances and Disease Registry (ATSDR), ”PCBs tend to accumulate in breast milk fat,” with accumulations increasing with the woman’s age. (82a) A study cited by the ATSDR showed how concentrated PCBs can become in breast milk: “Daily PCB intake for native northern Quebec women was calculated to be 0.3 μg/kg (ppb) body weight while daily intake among infants was calculated to be 10 μg/kg due to breast feeding.” (Section 6, p. 584) That means that, at least as found in this study, toxins that enter the woman’s body are excreted in breast milk in what is effectively a 30-times-higher concentration compared with their entering concentration. A study in the Netherlands, also summarized by the ATSDR (p. 569), found that, at 42 months of age, the median plasma PCB levels of children who had been breastfed for at least 6 weeks were 4½ times as high as those of children who had been formula-fed. A commission of the German Federal Environmental Office reported that the average daily PCB intake of an adult is 0.02 micrograms 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.(82c)
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 have 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, "Much higher doses of organochlorine compounds (from 10 to 20 times higher) penetrate the infant's body via the milk than via the transplacental route." (81b) (note that PCBs and dioxins are included among organochlorine compounds)
For further evidence of efficiency of lactation as a means of concentrating environmental toxins: Below will be information about benzo(a)pyrene (BaP), a Class 1 carcinogen, which was found to be taken in by infants of urban smokers via breast milk in doses up to 1000 times higher than was normal for infants of rural non-smokers.
Compared with bottle-fed infants:
According to an EPA report, providing estimates for typical exposure in the U.S. based on EPA data but also drawing on studies of populations in Germany (two studies), Britain and the Netherlands, "Breast-feeding for 6 months or more is predicted to result in an accumulated (dioxin) exposure 6 times higher than a formula-fed infant during the infant's first year of life.”. (83) 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. (85) This study (Abraham et al.) was cited in a 2002 EPA document ("Infant Exposure to Dioxin-like Compounds in Breast Milk") that apparently considered it to be fully valid. (37a) The figures of 10 times lower concentration for formula-fed at 11 months and 6 times higher accumulated exposure for breastfed are mutually compatible, given the differences in what was measured. And both figures are compatible with the up-to-50-times-higher figure for intake of breastfed infants compared with formula-fed, given that transmission of toxins starts out higher but declines substantially over the course of a year as the mother's stores of the toxins are excreted.
However, the 6- or 10-times-higher range of accumulation or concentration in the breastfed infants may understate the reality of the harm caused, since the "up to 50 times higher" short-term exposure may result in unusual harm just during that short-term period.
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 children who had been breastfed for at least 12 weeks were still over twice as high as in bottle-fed children at 7 years of age, in an American/German study. (82b)
The above has focused on the unusually high concentrations of dioxins and PCBs in human milk, but there are also almost certainly the same kinds of higher concentrations of other toxins in human milk as well, as compared with those toxins in cows' milk, for the following reason: In the cases of toxins taken in by inhalation (including PAHs from diesel emissions and smoking, various chemicals from residential wood burning, and other vehicle emissions-- see later in this section), it is safe to assume that human mothers would have far more exposure to those toxins than would cows.
Diesel emissions, Tobacco Smoke, and PAHs:
Note that diesel engine exhaust was classified as a known human carcinogen by the EPA in 2012. One of the toxic components (in addition to dioxins) known to be contained in the rising diesel emissions, PAHs (known to cause cancer in animals), has almost certainly also continued to increase in atmosphere inhaled by many nursing mothers and mothers-to-be. Note in the next paragraph how closely PAH concentrations in breast milk are related to exposure to diesel exhaust.
The chart on the left (from a Japanese study) indicates high concentrations of five different kinds of PAHs in breast milk of rats that had been exposed to diesel exhaust (DE) for six hours a day from the seventh day of gestation until 14 days after birth, with concentrations similar to those in downtown Kanazawa, Japan37b (Kanazawa is the study's lead author's university city, population 450,000). PAH concentrations in the breast milk of the exposed rats ("DE") were two to three times higher than in the control group, despite the fact that the exposure was apparently only moderately high; note that this exposure of the rats to diesel exhaust, for only six hours a day, was not an especially high dosage. As indicated in this chart, lactation appears to be an efficient means of taking in toxins from the atmosphere and concentrating them in breast milk. Although information about PAHs in cow's milk does not appear to be available for comparison, it is probably safe to assume that a much higher percentage of human mothers and mothers-to-be than of cows has a close exposure to diesel exhaust, from vehicular traffic, railroads, ships, port and canal dredging machinery, construction equipment, etc.
There is apparently no data available about diesel exhaust in breast milk, which may be due to difficulty of quantifying a substance in breast milk that is specifically identifiable as diesel exhaust, given the fact that such exhaust consists of many different chemicals. But bear in mind the high levels of two of the important components of diesel exhaust that are known to be present in breast milk:
(a) the known carcinogen and neurodevelopmental toxin, dioxin, in high concentrations (see earlier in this Section), and
(b) PAHs (see earlier about PAHs being known to cause cancer in animals).
Since two of the distinct toxic components of diesel exhaust are each known to be heavily present in breast milk, it is reasonable to suspect that the "diesel exhaust" category also, with its own separately-known carcinogenicity and endocrine disruption properties,(90b) is also essentially present in breast milk.
An Italian study found PAHs to be higher in lactating women who smoke. The specific form of PAH that was investigated in this study was benzo(a)pyrene (BaP), which is classified as a Class 1 carcinogen by the International Agency for Research on Cancer. There is no determination of a maximum tolerable amount in breast milk, so the Acceptable Daily Intake (ADI) for drinking water was used in the study. "For babies whose mothers belonged to the non-smoker rural category, daily BaP equivalent intake during a six-month nursing period was below the ADI." But intake of BaP in breast milk by infants of urban smokers showed values "from about seven times, up to 1000 times higher than ADI." (emphasis added) Breast milk of urban non-smokers was intermediate in concentrations.(26a) Note that BaP is also a major component of diesel exhaust,(90c) as well as of tobacco smoke.
Authorities writing about dioxins emphasize the predominant role of diet as being the major source of those toxins into the body (and thereby into breast milk). It is worth taking special note of the fact that, in the cases of the also-toxic PAHs from diesel exhaust and tobacco smoke (as indicated above), the inhalation route is also an important means of absorbing environmental toxins which can then become highly concentrated in breast milk.
The above two studies appear to be the only ones published regarding presence in breast milk of PAHs (including BaP). They show carcinogens and probable developmental toxins being found especially concentrated in breast milk following rather ordinary exposures of the mothers to diesel emissions and tobacco smoke. The amount of PAHs in the breast milk was directly related to the extent of the mothers' exposures to the chemicals. The finding of carcinogenic intake of BaP by breastfeeding being up to 1000 times the acceptable level for infants of urban smoking mothers, while levels were in the safe range for rural non-smokers, highlights how extremely effective lactation is at taking in environmental pollutants in typical amounts and concentrating them in breast milk.
Mothers should not necessarily feel safe about their breast milk if they are rural non-smokers. Whereas PAH's are apparently mainly taken in by inhalation, dioxins are mainly taken in by way of food; unless one lives in an unusually low-pollution food-source region, the only way to avoid typical concentrations of dioxins in breast milk is to adopt a basically vegetarian diet many years before breastfeeding starts. Also, residential wood-burning emissions are a major source of BaP,(26b) typically emitted in the immediate air supply of both lactating mothers and infants. Breast milk in rural Italian mothers was probably uniformly within acceptable limits of BaP at least partly because there is relatively little residential wood burning in sunny Italy, with minimal forests. It is also important to bear in mind that backyard burning, often done in rural areas, has become the largest single source of releases of dioxins to the atmosphere in recent years, according to the EPA.
Thinking about the up-to-1000-to-1 ratio of BaP in breast milk of urban smokers vs. that in rural non-smokers, it is not hard to guess which end of that ratio the milk of cows would be closer to. And relatively few human mothers in industrialized countries would be likely to have milk at the rural end of the ratio. Residential wood-burning pollution would be another source of toxins that would have little effect on cows' milk but considerable effect on the milk of many women.
In Section 4.4 of the EPA's 2002 Health Assessment Document for Diesel Engine Exhaust, it is pointed out that, "Extensive studies with salmonella have unequivocally demonstrated mutagenic activity…. Several of the chemicals found in diesel emissions possess mutagenic activity in a variety of genetic assays."
Diesel emissions from trucks and trains are especially likely to be harmful because they are released (a) close to ground level and (b) from large numbers of exhaust pipes that are travelling thousands of miles on roads and tracks that are widely distributed within populated areas. Those emissions quickly and directly reach the air breathed by many infants and childbearing women, and their particulate matter lands on surfaces crawled on by many infants, as well as on objects handled and mouthed, and on soil that could then be ingested by infants.
Marine diesel emissions aren't normally released as closely into populated areas as diesel emissions from trucks and trains (and many European cars), but they are nevertheless often released very near to populated areas. Probably the outstanding example of this is the state of Louisiana, as seen on this map showing the locations of Louisiana's ports. Just one of these ports (Port of South Louisiana, marked on lower right of this map) is the largest tonnage port in the entire western hemisphere. The ports of New Orleans and Baton Rouge are also major ports. And there are also 29 other ports in Louisiana, many of them on inland waterways, most of them well within populated areas. Since marine fuel is diesel, and considering all of the diesel-powered loading/unloading machinery, dredging equipment, and diesel trucks and trains going to and from these ports, it is almost certain that Louisiana is the U.S. state whose population is most heavily affected by diesel emissions. Bear that in mind when remembering or looking at the map (Fig. 4) of cancer incidence by U.S. states as shown in Section 1, in which there is only one orange-colored (high-cancer) state in the entire 3/4 of the U.S.A that is outside the northeastern quarter of the U.S.: that state is Louisiana.
The "bunker" type of fuel that is used in ships and for heating in some large urban buildings is an atypical form of diesel fuel. Most people are surprised to learn that the EPA has calculated that many thousands of deaths occur in North America every year as a result of diesel emissions from ocean-going ships,(200), although substantial death rates have also been attributed to land-based diesel emissions (per EPA announcements). An EPA document regarding diesel pollution from ocean shipping points out that the PM contained in marine diesel emissions includes dioxin. (201). It also points out that "Marine diesel engine emissions consist of a higher fraction of ….. metallic ash (approximately 7-11%) than (is) typically found in land-based engines".(202) The higher proportion of metallic ash in marine diesel emissions is especially important because formation of dioxins during combustion is promoted by metals' acting as catalysts during the combustion. (204) Between the above and the presence of sodium chloride in sea air (as a source of the chlorine needed to form dioxins during normal combustion), marine diesel emissions may be substantially higher in dioxins than is average for other diesel engine exhaust.
Household smoking: For information about general adverse health effects on children (especially SIDS) in households in which smoking is done, see Appendix 1, Section D of www.breastfeedingprosandcons.info/. Carcinogens and particulate matter are only part of the many toxins known to be present in tobacco smoke. A study dealing with PAHs, which are known carcinogens and which have been found in breast milk in greatly varying amounts according to extent of household smoking, was discussed earlier.
Alleged decline of dioxins in breast milk
Declining (??) dioxin levels in breast milk? People who promote as-exclusively-as-possible breastfeeding often quote a World Health Organization (WHO) study finding that toxin levels in breast milk have been declining "in most industrialized countries;" but the U.S. is conspicuously absent from the data provided by WHO, including in all documents found in a detailed search of WHO's website in January of 2012. The European countries, data for which WHO does provide, have been more aggressive than the U.S. in combating pollution, from diesel combustion sources especially. Measurements of dioxin emissions per liter of diesel fuel consumed show far higher rates in the U.S. than in the European countries where tests were conducted (Germany and Belgium).(257a) The emission differences may be accounted for by the differences in regulation (annual emissions inspections normally required in the EU, not in the U.S.); the only readily-found study comparing dioxin emissions from diesel engines of different conditions determined that a "high-mileage" diesel engine emitted almost three times as much dioxin toxic equivalency as a newly-rebuilt engine. (257b)
Dioxins from diesel emissions have been rapidly rising in the U.S., according to the most recent EPA data; this is especially significant in that diesel emissions are very often released intensively at ground level within densely-populated areas; that is unlike the major smokestack sources, which are the emitters whose releases have declined. Authors looking for trends in dioxin levels in breast milk for the U.S. sometimes say that the trend here is "ambiguous," or they tell only about the finding concerning "most industrialized countries," implying that the U.S. would be in that category. "Ambiguous" seems to be a word that avoids recognizing an upward trend in the U.S., unless data can be shown other than what is shown in this chart; substantial searching by this author has been unable to find anything else. (Note that observations for the U.S. are shown with the darker dots on this 2001 chart.)
Residential wood burning, wildfires, and pesticides as sources of carcinogens
Foliage and wood (as well as fossil fuels) contain the three elements which, when chlorine is present during combustion, can produce dioxins.
The final ingredient (chlorine) can be provided by atmospheric pollutants and especially by the plastics contained in typical trash. This potential for creating dioxins during burning of organic matter is present even when the fuel doesn't already contain toxins. But in addition, vegetation also typically absorbs and retains existing toxins (which can be re-suspended during burning). It appears to be generally agreed, including in research by NASA, that many houseplants are effective at reducing indoor pollution because they absorb toxins from the air (through openings normally on the undersides of the leaves). Outdoor vegetation can be expected to do that same absorption of toxins. The toxins will probably remain contained within the plant or tree, continuing to accumulate through the years for longer-lived vegetation. Those stored toxins will almost certainly be dispersed into the air when the vegetation is burned during wildfires. (Obviously, the effect would be reduced if some toxins had travelled to the roots.) Preservative-treated wood contains dioxins, which would greatly increase the toxic effects of any such burning. So residential burning as well as wildfires could be expected to be substantial sources of toxins able to be re-suspended into the air, especially if much of the vegetation burned is years old. This re-suspension is in addition to the creation of dioxins that takes place as a result of the burning.
Residential burning is especially likely to create toxins if it isn't done correctly, and it probably isn't done correctly a very high percentage of the time. The recommendations for burning so as to avoid creation of toxins are probably not widely observed by the wood-burning public; those instructions include keeping the fire hot, and not allowing it to smolder (which probably stems at least in part from the fact that dioxins form most efficiently in the lower end of normal combustion temperature ranges). One may wonder how often a fire is kept hot during an evening that is chilly but not cold, as well as how hot a fire stays while unattended overnight in a home that relies on wood for its main source of heat.
Pesticides also, including some that are used residentially, have been widely found in breast milk.(92). As explained above, breast milk today is not the beneficial, safe substance today that it was in earlier times: Essentially all of the above toxins have begun to become major problems in the environment only beginning in the mid-20th-Century, with some of them (such as BPA and some pesticides) not becoming significant until very late in the 20th Century. Many new types of pesticides were introduced only in the 1980's..(92)
A study of effects of proximity to California freeways found a doubled risk of autism among infants residing within about 1000 feet of a freeway. (194) Beyond that (for the approximately-three-mile width of the area studied), there seemed to be little change in autism levels depending on distance from the freeway. But the study was conducted in what is considered by the Census Bureau to be urban areas, where general pollution levels are normally high compared to non-urban areas. Greater distances from busy highways (beyond the 1000-foot threshold) would almost certainly be found to have beneficial effects if the region studied were to extend into non-urban areas that don't have their own serious pollution sources.
The big question is the distance that non-road combustion emissions will travel and still seriously affect people. As opposed to vehicular emissions that originate very close to ground level and therefore affect people nearby, emissions from tall smokestacks from power plants, large factories, and large ships are initially emitted high above the surface and are directed upward; then the heat of the emissions keeps carrying them still farther upward for some time after exiting the stacks. The wind carries them for many miles, until eventually major parts of the emissions are deposited onto surfaces. Some are likely to be deposited relatively nearby, possibly starting a few miles downwind from the source. The EPA has formally acknowledged significant pollution in Pennsylvania, New York, and the New England states resulting from sources up to 550 miles away. (264)
In addition to the more or less gradual effects of gravity, precipitation considerably accelerates deposition of pollutants. That helps explain why the drier states generally have low autism and cancer rates, with the exception of very-high-breastfeeding Utah.
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(26) Being breastfed in infancy and adult breast cancer risk among Japanese women Y. Minami/ M. Kawai (Division of Community Health, Tohuku University Graduate School of Medicine) et al. Cancer Causes Control, 2012
(26a) Chemosphere. 2007 Apr;67(7):1265-74. Epub 2007 Jan 26. Polycyclic aromatic hydrocarbons (PAHs) in human milk from Italian women: influence of cigarette smoking and residential area. Zanieri L, et al., University of Florence, Department of Chemistry, Florence, Italy. At http://www.ncbi.nlm.nih.gov/pubmed/17258279
(27) Chemosphere. 1996 Feb;32(3):543-9. Decrease in milk and blood dioxin levels over two years in a mother nursing twins: estimates of decreased maternal and increased infant dioxin body burden from nursing. Schecter A, Papke O, Lis A, Ball M, Ryan JJ, Olson JR, Li L, Kessler H Department of Preventive Medicine, State University of New York, Health Science Center-Syracuse, USA
(27-0) Dioxin emissions from a municipal solid waste incinerator and risk of invasive breast cancer: a population-based case-control study with GIS-derived exposure Jean-François Viel, et al. International Journal of Health Geographics, 2008, Volume 7, Number 1, 4
(27a) Do Human Milk Concentrations of Persistent Organic Chemicals Really Decline During Lactation? Chemical Concentrations During Lactation and Milk/Serum Partitioning, Judy S. LaKind et al. Environmental Health Perspectives http://ehp03.niehs.nih.gov/article/fetchArticle.action?articleURI=info:doi/10.1289/ehp.0900876
(27e) 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
(27f) Surgeon General's Call to Action to Support Breastfeeding 2011
(27g) M A Mascola,et al., Exposure of young infants to environmental tobacco smoke: breast-feeding among smoking mothers. Am J Public Health. 1998 June; 88(6): 893–896. PMCID: PMC1508233 found at www.ncbi.nlm.nih.gov/pmc/articles/PMC1508233
(28) ATSDR web page "Public Health Statement for DDT, DDE, and DDD,"September 2002, Section 18.104.22.168 at http://www.atsdr.cdc.gov/toxprofiles/tp35.pdf
The exact wording that was paraphrased here was, "The proper development of many systems and functions depends on the timely action of hormones, particularly sex steroids; therefore, interfering with such actions can lead to a wide array of effects that may include altered metabolic, sexual, immune, and neurobehavioral functions. Effects of this type, that occur following exposure during fetal life via the placenta or early in life caused by either direct exposure to chemicals or exposure via maternal milk, are discussed in this section."
(34) ATDSR document on dioxins, section on environmental sources
(34a) National Academies of Science report on dioxins in the food supply. http://books.nap.edu/catalog.php?record_id=10763
(34b) 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." 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.”
(34c) U.S. EPA. Estimating Exposure To Dioxin-Like Compounds - Volume I: U.S. Environmental Protection Agency, Washington, D.C., EPA/600/8-88/005Ca., 2002, revised 2005 – http://cfpub.epa.gov/si/si_public_record_Report.cfm?dirEntryID=43870, Section II.6, "Highly Exposed Populations" (nursing infants are considered to be one of the highly-exposed populations), 4/94 (p. 39) "Using these procedures and assuming that an infant breast feeds for one year, has an average weight during this period of 10 kg, ingests 0.8 kg/d of breast milk and that the dioxin concentration in milk fat is 20 ppt of TEQ, the average daily dose to the infant over this period is predicted to be about 60 pg of TEQ/kg-d."
(34d) Schecter, A., et al. Chlorinated Dioxins and Dibenzofurans in Human Tissue from General Populations: A Selective Review, Environmental Health Perspectives Supplements 1994; 102(Supple 1): p. 159-171 and Schecter, A., et al. Congener-specific Levels of Dioxins and Dibenzofurans in U.S. Food and Estimated Daily Toxic Eequivalent Intake, Environmental Health Perspectives Journal 1994; 102(11): p. 962-966.
PCDDs, PCDFs, and PCBs concentrations in breast milk from two areas in Korea: body burden of mothers and implications for feeding infants, Jiyeon Yang et al. Chemosphere 46 (2002) 419–428
(36) Executive Summary: Assessment of the health risk of dioxins: re-evaluation of the Tolerable Daily Intake (TDI) WHO Consultation May 25-29 1998, Geneva, Switzerland, p. 27
(37a) Infant Exposure to Dioxin-like Compounds in Breast Milk Lorber1 and Phillips2 VOLUME 110 | NUMBER 6 | June 2002 • Environmental Health Perspectives http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download
(37b) Transfer of Polycyclic Aromatic Hydrocarbons to Fetuses and Breast Milk of Rats Exposed to Diesel Exhaust, Tozuka, Watanabe et al., Kanazawa University and Tokyo Metropolitan Public Health Research Institute; Journal of Health Science 50(5) 2004 pp. 497-502
(81b) Concentration of Persistent Organochlorine Compounds in the Placenta and Milk of the Same Women, Katarzyna Czaja et al., Ch. 21 of Persistent, Bioaccumulative, and Toxic Chemicals I, Robert L. Lipnick et al. editors, ACS Symposium Series, American Chemical Society, 2001; citing Jensen, A.A. et al, Chemical Contaminants in Human Milk, CRC Press, Inc., Boca Raton, Ann Arbor, Boston, 1991. 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
(82) National Academies Press: Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment (2006), Board on Environmental Studies and Toxicology, National Academy of Sciences; the original source is not quoted directly because it is part of a draft, not for quoting
(82a) ATSDR Public Health Statement for Polychlorinated Biphenyls (PCBs), November 2000, Balfanz et al. 1993; MacLeod 1981; Wallace et al. 1996, p. 569
(82b) Pediatric Research (2001) 50, 331–336; doi:10.1203/00006450-200109000-00007 Early Childhood Determinants of Organochlorine Concentrations in School-Aged Children, Wilfried Karmaus et al.
(83) Infant Exposure to Dioxin-like Compounds in Breast Milk, Lorber and Phillips Volume 110 | Number 6 | June 2002 • Environmental Health Perspectives http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download 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.
(85) 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
(89) "Paying a Price for Loving Red Meat" in Personal Health, by Jane E Brody, New York Times: April 27, 2009
(90b) Particle and Fibre Toxicology, Effects of prenatal exposure to diesel exhaust particles on postnatal development, behavior, genotoxicity and inflammation in mice. Karin S Hougaard et al., National Research Centre of the Working Environment, Copenhagen, Denmark. Published: 11 March 2008 Particle and Fibre Toxicology 2008, 5:3 doi:10.1186/1743-8977-5-3 This article is available from: http://www.particleandfibretoxicology.com/content/5/1/3
(92) http://ehpnet1.niehs.nih.gov/docs/2001/109p75-88lakind/abstract.html Environmental Health Perspectives, Vol. 109, No.1, Jan. 2001
(106b) Cancer Treat Rev. 2010 Jun;36(4):277-85. Epub 2010 Mar 15.Epidemiology of childhood cancer. Kaatsch P. Institute for Medical Biostatistics, Epidemiology and Informatics, University of Mainz, Germany. (http://www.ncbi.nlm.nih.gov/pubmed/20231056 )
(106b1) Parking DM et al., International Incidence of Childhood Cancer IARC scientific publication, Vol. II. Lyon: International Agency for Research on Cancer, 1998 p. 144, quoted in Kaatsch Peter, Epidemiology of childhood cancer Institute for Medical Biostatistics, Epidemiology and Informatics, University of Mainz, Germany, Cancer Treatment Reviews 36 (2010) 277-285 High-breastfeeding countries listed were Sweden, Norway, Denmark, Finland, Italy, Spain, New Zealand, Australia, and Germany. No data for Belgium.
(106c) Childhood cancer epidemiology in North America, Logan Spector, PhD, Univ. of Minn, citing Pizzo and Poplack, 2002, and SEER AYA monograph;. also “Childhood cancer rates rise in Europe”, in The Guardian, U.K., 9 December 2004)
(106c2) Little J., Epidemiology of Childhood Cancer, IARC Scientific Publications No. 149, Lyon; International Agency for Research on Cancer, 1999; cited in "Trends in childhood cancer incidence in Europe, 1970-99", Steliarova-Fourcher et al., on behalf of the ACCIS Scientific Committee, in www.thelancet.com, Vol. 365, June 18, 2005, p. 2088
Published online 2011 August 17. doi: 10.1016/j.canlet.2011.08.003 PMCID: PMC3185182 NIHMSID: NIHMS320383
(106c2a) Steliarova-Fourcher et al., Geographical patterns and time trends of cancer incidence and survival among children and adolescents in Europe since the 1970s (the ACCIS project): an epidemiological study. www.thelancet.com Vol. 364, Dec. 11, 2004
(106c2b) Karim-Kos HE, et al., Recent trends of cancer in Europe: a combined approach of incidence, survival and mortality for 17 cancer sites since the 1990s. Eur J Cancer. 2008 Jul;44(10):1345-89. Epub 2008 Feb 14 at http://www.ncbi.nlm.nih.gov/pubmed/18280139. Ann Oncol. 2003 Aug;14(8):1312-25. Measuring progress against cancer in Europe: has the 15% decline targeted for 2000 come about? Boyle P, et al. http:/www.ncbi.nlm.nih.gov/pubmed/12881398
Source for other text at about this point: (http://www.atsdr.cdc.gov/com/cancer-fs.html)
(106c2c) Breastfeeding data from CDC's "Breastfeeding among U.S. Children Born 2000-2009," CDC National Immunization Survey, averaging 2001-2003 years' data for "Ever" breastfed, breastfed at 6 months, and breastfed at 12 months.
(106c3) Birth characteristics and brain cancers in young children, Julie Von Behren et al., International Journal of Epidimiology, Vol. 32 (http://ije.oxfordjournals.org/content/32/2/248.long) "With over 700 cases, this is one of the largest childhood CNS case-control studies to date." In the von Behren et al. study, children whose mothers were born outside the US appeared to have greatly reduced risk of central nervous system tumours (OR = 0.66, 95% CI: 0.55–0.80). Since mothers born outside the U.S. in recent decades have been predominantly from third-world countries (especially Hispanics), with far less lifetime exposure to and body accumulation of chemicals that have become widespread in developed countries in the last half century or so, their breast milk would be expected to have much lower levels of dioxins and other known or likely carcinogens. Breastfeeding rates of Hispanic women (especially those from Central American and the West Indies – see Section 4 of www.causeofdiabetes.net ) are also lower than those of non-Hispanic whites, and their diets are higher in grains and legumes and lower in dioxin-containing fat and dairy products than the typical non-Hispanic diet.
(106c4) NCI data quoted on a George Mason University website at http://stats.org/stories/2010/childhood_cancer_may28_10.html
(106c5) J Neurol Neurosurg Psychiatry 2004;75:ii12-ii17 doi:10.1136/jnnp.2004.04074, Brain tumours: incidence, survival, and aetiology, Table 2, at http://jnnp.bmj.com/content/75/suppl_2/ii12/T2.expansion.html Factors researched include ionizing radiation, mobile phones, extremely low frequency electromagnetic fields, viruses, atopy, nitrosamine/nitrite/nitrate, aspartame, tobacco, alcohol, hair dyes, solvents, pesticides, traffic-related air pollution, rubber and vinyl chloride manufacture, petroleum refining, head injury.
(106d) http://www.qub.ac.uk/research-centres/nicr/FileStore/PDF/Filetoupload,176738,en.pdf, (Queens University Belfast) Figure 4.4: "International comparisons of world age-standardised incidence rates for childhood cancer: 1998-2000." We averaged the cancer rates for boys with the rates for girls for each country. The low-breastfeeding countries were U.K., Ireland, France and Belgium, and the high-breastfeeding countries were Denmark, Germany, Austria, Australia, Sweden, Spain, Finland and Italy; Denmark was the only country with a prevalence below the highest prevalence among the low-breastfeeding countries, and that was only 0.05 lower)
(146) See Figures 1.8 and 1.9; Also data provided by LaLeche League for Northern Ireland, accessed at http://www.lalecheleague.org/cbi/bfstats03.html, in line with data for Dublin area from: Public Health Nutrition. "Breast-feeding practices in Ireland", Tarrant RC, Kearney JM., School of Biological Sciences, Dublin Institute of Technology, Republic of Ireland, accessed at Proc Nutr Soc. 2008 Nov;67(4):371-80. Epub 2008 Aug 20.
(147) http://www.aactionautism.org/node/152 Also Research to determine autism incidence [Posted: Fri 03/04/2009 by Deborah Condon http://www.irishhealth.com/article.html?id=15312&ss=autism
(154) “Report on a WHO/UNICEF consultation for the WHO European region for the development of a global strategy on infant and young child feeding, Budapest 28 May- 1 June 2001”, Table 5.1
(155) data from CDC Summary, cited above
(194) "Residential Proximity to Freeways and Autism in the CHARGE Study" , Environmental Health Perspectives, Published in 119(6) Jun 2011, Heather E. Volk, Irva Hertz-Picciotto et al., reported (with doubling comment) in ScienceDaily (Dec. 17, 2010), "Proximity to Freeway Associated With Autism"
(200) “Proposal of Emission Control Area Designation for Geographic Control of Emissions from Ships”, EPA-420-F-09-015, March 2009; the complete, lengthy document can be read online at http://www.epa.gov/nonroad/marine/ci/420f09015.htm .
(201) EPA's Proposal to Designate an Emission Control Area for Nitrogen Oxides, Sulfur Oxides and Particulate Matter,Technical Support Document Chapter 3: Impacts of Shipping Emissions on Air Quality, Health and the Environment
(202) 22.214.171.124 of same proposal
(203) ”Research findings on particulate air pollution from the Southern California Particle Center", John R. Froines, Ph.D., Director, presented at EPA webinar Dec 8, 2010, found at http://www.epa.gov/airscience/seminars/SCPCwebinar8Dec10.pdf
(204) EPA/600/P-03/002F November 2006, p. 2-2
(205) found at http://www.epa.gov/mercury/effects.htm
(257a) C.A. Laroo et al., Emissions of PCDD/Fs, PCBs and PAHs from a Modern Diesel Engine Equipped with Catalyzed Emission Control Systerms, Environmental Science and technology, ACS Publications, June 30, 2011
(257b) Gullet, B.K. et al., On-road emissions of PCDDs and PCDFs from heavy duty diesel vehicles, Environ. Sci. Technol., 2002, 36, 3036-3040
(24a3) Broadening the Perspective of Pica: Literature Review ELLA P. LACEY, PhD at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1579989/pdf/pubhealthrep00198-0031.pdf