Comments on Research by Case and Deaton concerning Health Declines and Reductions in Life Expectancies among U.S. Whites


Evidence indicates that certain chemicals (PCBs and dioxins), which became widespread in the mid-20th-Century U.S., may have contributed to health declines and reductions in life expectancies among U.S. whites, such as described by Case and Deaton.17b  Exposures to those toxins (now recognized to have health effects related to these problems) increased greatly at specific times compatible with the beginnings and increases of the health declines.  Significant exposures took place in mid-century and later, when children could have been exposed to those chemicals in concentrations thousands of times higher than the level that the EPA currently considers to be safe; and those exposures took place during vulnerability of development.  The children most affected by PCBs would have fitted (in ethnicity, nationality, and likelihood of graduating from college) the profile of the group that would later, in midlife, have high and increasing deaths of despair.


Readers please note:  A much-improved version of the rest of this article has been completed, one that is better organized, more concise and more complete than what follows below.  The reader may prefer to go directly to that (at at this point.



Section 1:  Beginnings and increases in adverse trends:

Fig. 1



Notice in this graph (from a 2017 document by Case and Deaton1d) that, following insignificant changes in drug, alcohol and suicide mortality in 1935-1940, there were

    (a) a minor increase with the 1945 cohort and

    (b) major mortality increases among those born in (about) 1950 and later.



Confirming this time trend with a different dataset, see (on the right) what happened when U.S. whites who were born at different times around the mid-20th century arrived in the 50-to-54 age category.  If they were born in 1940, mortality data for this age group would be found at the 1990-1994 position, when deaths of despair among U.S. whites were fairly stable (see left end of red line).  


But that slowly changed to

    (a) minor increases among those born during the 1940's, and

    (b) major increases among those born about 1950 and later.  Data for people (age 50-54) born in 1950 would be in the 2000-2004 part of  the red line, where we see established, rapidly increasing mortality, which continued to rapidly increase as far as the data continues.


So there apparently was a major transition in which lives of many children born and developing in the U.S. during the 1940's, and especially those born closer to 1950 and later, would end up worse than those of similar people born in earlier years and in other countries.  For additional data implying that this was a period of transition that can help explain midlife health problems, see Appendix A.


Infancy and early childhood are known to include "critical windows of vulnerability" of development, when toxins can cause adverse later outcomes.1  Given that, and also considering the decline in health among people born in the years indicated above, we should look into any toxins that (a) were increasingly appearing in the environments of developing U.S. children during the 1940's and (b) became more prominent in the environment about 1950 and later.


PCBs (polychlorinated biphenyls),  which the U.S. ATSDR (Agency for Toxic Substances and Disease Registry) now ranks among the top five priority hazardous substances,1c fit that descriptionUse of PCBs (not yet known to be toxic then) increased during the 1940's, especially after 1945.1e   They were used in various areas of manual work, especially in the U.S.7   Exposures became much greater in 1949 and later, when PCBs came to be used in various types of building materials.4  A 2012 study stated that volatilization of PCBs from building materials has been reported to produce PCB levels in indoor air up to four orders of magnitude greater than levels typical of ambient air (citing five studies as evidence).1f  Construction workers would have brought these chemicals into their homes on their skin and clothing, exposing their families.1b   In relation to the greatly increased "deaths of despair" in midlife recently reported by Case and Deaton, childhood exposures to PCBs are known to have effects that can lead to pain in adulthood.  (Details follow.)


Section 2:  Why focus on early childhood exposures of the people who were later to have deaths of despair?


A publication of the U.S. National Academies Press refers to "specific periods in development when toxicity can permanently alter the function of a system at maturity. These special windows of vulnerability (critical periods) ...  may demonstrate particular sensitivity during the postnatal period."1g (italics added)  Publications of the World Health Organization point out that "Many adverse environmental exposures such as to chemicals during childhood lead to disease or early death at adult age;" 2 and such exposures can lead to adverse health outcomes "throughout the lifespan."2a   Another WHO publication also states that "environmental exposures (in early life) can induce various epigenetic processes which alter disease susceptibility."2  A group of over 20 experts, many of whom are highly published authors, stated in 2008 that "studies in a variety of species of experimental animals indicate polychlorinated biphenyls (PCBs) to be highly immunotoxic," referring to early life exposures to PCBs as having that effect. 3  It should be reasonable to assume that reduced immunity to disease (possibly caused by childhood PCB exposure) could lead to adult pain as well as to more serious consequences in later life.  Other effects of childhood exposures to PCBs that may lead to despair in later life will be presented later.


Of the scores of former applications of PCBs, their use in building materials (which began in 19494) would have led to especially high exposures of children.  Many people living, working, or attending school in buildings constructed with the PCB-containing materials would have been closely exposed, as would people working with those materials. The maximum PCB concentration that the EPA currently allows in building materials is 50 parts per million,5b as compared with the 40 parts per hundred that were used in some building materials at that time5 -- 8,000 times the current maximum set by the EPA.  PCBs emitted from building materials have been found to lead to major increases in blood levels of PCBs.4a  Children may often have gone through their windows of developmental vulnerability while exposed to increasing levels of PCBs during the 1940's, via air and dust and by personal contact with family members,1b with especially great increases in 1949 and later when PCBs were used in building materials.


Even after new manufacture of these chemicals was banned, thousands of spills of PCBs during handling and transport were reported to the EPA;8 and that included only spills that (a) were reported to the EPA, and (b) that involved over one pound of PCB.  When noting that many thousands of pounds of PCBs have been spilled in the U.S., we should be aware that less than 1/100,000th of an ounce of a PCB-containing product administered per day to pregnant and lactating female monkeys was found to cause the 6-to-24-month-old offspring to be hyperactive.9  Apparently even miniscule amounts of these toxins can have adverse neurological effects on primates, if the exposure is during development; and those effects can apparently endure into later life. That should be considered when thinking about what might have caused some people to feel badly in adulthood and to seek comfort in substances intended to relieve bad feelings.



Section 3:  Disproportionate exposures to PCBs in the U.S. compared with other countries, in three respects: 


Case and Deaton point to the high level of indications of feelings of despair in the U.S., compared with those in six other rich countries that have gone through similar economic stress.  Those differences might be explainable by

    (a) greater past use of PCBs in the U.S.:  The U.S., with (in 1960) 6% of the world's population,12 produced half or more of all PCBs produced in the world;1e,7,10  and 89% of U.S. production was used in the U.S.8  

Fig. 3

worldTempMap.jpg     (b) According to a study referred to in an EPA document, "the PCB emission rate is highly dependent on temperature," with a 400-fold increase taking place as the temperature increased from 30 to 50 degrees C"8f (86 to 122 degrees F).  With that in mind, see in this summer temperature map the redness of the U.S. as compared with the lack of redness in Canada and in all four of the European countries with whose more favorable mortality trends Case and Deaton compared the unfavorable trend in the U.S.;  those European countries are all located north of the only red areas shown in Europe.


When looking at this map, one should remember that, for decades during the sensitive developmental periods of today's mid-life people (Section 1), building materials were used that exceeded the current EPA maximum for PCBs by thousands of times (Section 2), and the PCB emission rate apparently increases dramatically at higher temperatures. 


     (c) National differences in deaths of despair may also be explainable partly on the basis of specific applications in which PCBs were usedthere was at least one PCB application that was unusually widespread in the U.S. --  that of asphalt roofing materials.8a  A substantial amount of PCB-containing material directly above the heads of many people would be especially significant in that PCBs form vapors that are heavier than air.8b   An industry source says that most estimates consider asphalt shingles to hold over 80% of the U.S. residential market,8c and ample casual observations in the U.S. seem to confirm that figure.  But it is very different on the European continent. (See below)

Fig. 4


So grey slate roofs in northern France give way to terracotta in southern France.  In Germany (see below) slate and tile roofs appear side-by-side.  In Sweden, most roofs are apparently tile or metal.8h  Asphalt shingles don't seem to be a significant part of the picture in continental Europe.


 Fig. 5



And asphalt shingles are not even among the top three types of roofing materials in Australia,8d another of the comparison countries that had much more favorable mortality trends than that of the U.S.


So people in four of the six comparison countries suggested by Case and Deaton (Germany, France, Sweden, and Australia -- see Figure 2) are likely to have had little of the substantial PCB exposure that could have come from the asphalt roofing that was widely applied in the U.S. in earlier decades; and all of those countries had far more favorable mortality trends than the U.S., in the period studied.  In the remaining two comparison countries (UK and Canada), asphalt roofing is fairly popular;8e and (not surprisingly) we see that the UK and Canada both had substantial unfavorable trends in the mortality that Case and Deaton studied (1d p.15).  The U.S., with its mostly asphalt roofing, had a corresponding mortality trend that was even more unfavorable than those in the U.K. and Canada; that would be understandable on the basis of higher temperatures in the U.S. compared with those in UK and Canada  (see Section (b) above).


Australia, also, had an unfavorable trend in this mortality, but in Australia's case the mortality increase took place despite a relatively minimal use of PCB-containing asphalt roofing in that country.8d  However, exposures to PCBs in Australia via their uses in other applications, including as fire retardants in ceiling tiles,8g might have been as harmful as exposures from roofing materials could have been in more temperate climates, because of the effect of the high summer temperatures in Australia; this would have amplified emissions from the other PCB sources. (See (b) above)


Shown below is an abridged version of Figure 2, with the mortality data lines cropped out for all countries except Canada and Australia.  Notice that, in the cases of both of those countries, mortality was declining until 2000 and then soon turned upward; this reinforces the idea that the underlying cause of the adverse outcomes, as in the U.S., may have been increases in exposures to toxins that were greatly increasing in the environments of all three of those countries at about the same time. 

Fig. 6


Remember from Section 1 that PCBs came into use in building materials in 1949,4 which could have affected the development of people who later were in their early 50's as of the year 2000;  those exposures to toxins during vulnerable early childhoods may well have led to adverse effects in midlife (see Sections 2 and 6).  Notice above that mortality in Canada, a friendly next-door neighbor of the U.S. and probably with similar timelines for modifications in use of building materials, turned upward at essentially the same time as mortality turned upward in the U.S. (see Figure 2).  On the other hand, the upturn in mortality in Australia was a few years behind the upturns in the U.S. and Canada; PCBs were apparently never produced in that part of the world,1e so Australia would be expected to have been somewhat behind North America in starting to use PCBs in building materials. (PCBs were imported to Australia and did, as of sometime during the 1950's, become significant contents of materials used inside buildings there.8j)

Fig. 7



The U.K. was the only country discussed that already had substantially increasing mortality well before 2000; see the UK trend line just above, compared with data for the other countries in Figures 2 and 6.  The U.K. increase, also, can be related to PCB exposures, in this case exposures that would have greatly increased a decade before the major increases in PCBs in other countries.   The U.K. 50-to-54-year-olds during the mid 1990's (toward the left end of this graph) would have gone through their vulnerable periods of early development during and not long after World War II.  Those years, when Britain was anticipating a German invasion and later becoming the staging area for the massive Allied invasion of Europe, would probably have brought high exposures of UK citizens to PCBs, because of the substantial application of that chemical to armaments and military equipment.  Among other such applications, PCBs were used in protective coatings (including coatings of tarpaulins and tents) because of their fire- and water-resistant properties.20  Very probably, no other nation (as of that time, at least) ever had so much presence of PCBs in open applications within a relatively small land area.  This may explain the very unusual increase in midlife mortality among people who went through their vulnerable developmental periods in the UK during the early and mid-1940's. 


Of the countries considered here, the U.S. was the  only country besides the UK in which mortality was not declining among those born in the 1940's.  The increase in the U.S. was minor, but that increase was nevertheless very significant in that even a slight increase was in contrast with the general downward trend in mortality (see Figure 2).  The U.S. increase also, as was the case with the UK's increase, may well have resulted from wartime exposures to PCBs in protective coatings and other military applications.  But in the case of the U.S., the emitting manufacturing, armaments and equipment were present in a large country, and the products were probably soon shipped overseas, compared with the more concentrated (and probably longer-term) exposures in the U.K.  So it should only be expected that the PCB exposures during the 1940's would have had greater effects on children developing in the U.K. than on children in the U.S., at that time.  That may explain the much steeper increase in mortality in the U.K. during the 1940's, as compared with the mild increase in the U.S.



Section 4:  Disproportionate effects of the toxins on whites compared with African-Americans and Hispanics  (as found by Case and Deaton.)



Remember (from Section 1) that mid-century was the time of rapid increase of children developing who would later be affected by despair.  Exposures of children to PCBs being newly emitted by building materials in 1949 and later4 would have been greater for children living or going to school in recently-built buildings; this in turn would have been more likely for the economically-favored ethnic group (non-Hispanic whites) compared with (disadvantaged) minorities.


In a different area, first note that other uses of PCBs were in transformers and other electrical equipment, hydraulic and heat-transfer fluids, caulk, lubricants, 8 insecticides,6 and many other industrial applications.4  Then note the Atlantic article entitled "The 33 Whitest Jobs in America," itemizing jobs in which whites comprise a percentage of the workers that is much greater than whites' percentage in the population.11  Of those "whitest" occupational categories, fourteen of them were ones that would have had unusually high exposures to materials that contained PCBs:  construction trades, engine mechanics, machine operators, farmers, radio technicians, steel workers, electricians, etc.  All of these workers (and their children, indirectly1b) would have been exposed to PCBs in materials that were part of work in those occupations in the mid-20th Century.

 Fig. 8

image014.gifAlso, considering that a major pathway for PCBs to developing children is through their mothers, prenatally and via breast milk,11a  we should note that

   (a) Mexican-American women aged 16 to 49 have been found to have blood serum concentrations of PCBs about half as high as those of non-Hispanic white women11b (possibly because of dietary differences, given that PCBs become concentrated in certain types of food and not in others),

   (b) African-American mothers breastfeed for long periods at about half the rate of white women.11c


Therefore developmental exposures of Hispanic and African-American children to PCBs would almost certainly have been much less than exposures of non-Hispanic white children. 


The charts on the left are part of the substantial evidence indicating that by far the largest part of exposures of developing children to PCBs are via breastfeeding.  For more on this matter, including other evidence of harmful developmental effects of PCBs, see Section 3.a of  




Readers please note:  A much-improved version of of this article has been completed, one that is better organized, more concise and more complete than what follows.  The reader may prefer to go directly to that (at at this point.




Section 5:  Disproportionate effects of PCBs on children of non-degree-pursuing families (Case and Deaton found that people without college degrees had higher rates of deaths of despair than college graduates)


College graduates would very seldom go into the trades that have had major contact with PCBs (see the "whitest" occupations, above).  Even after the initial work fabricating and installing PCB-containing products, workers in similar trades would be working with and repairing equipment still containing PCBs and also maintaining and renovating buildings in which PCBs were contained in the original materials. It is probable that people other than college graduates would normally have been not only the people doing that work but also the ones exposed to the many thousands of spills of PCBs that have occurred.8


All of these exposures of white U.S. working-class adults would have meant greater exposures of their children,1b during the children's critical windows of developmental vulnerability,1 very possibly leading to long-term effects that included pain when those working-class children became older. (more below)



Section 6:  Other effects of PCBs that could be unnoticed in childhood yet lead to pain and despair in midlife (in addition to reduced immunity to disease, as discussed earlier)


PCBs were found in a 2009 laboratory experiment (Seelbach et al.)14 to disrupt the blood brain barrier in animals; so exposures to PCBs in childhood might leave the brain unusually vulnerable to environmental toxins indefinitely, meaning that the future adult would encounter occupational and other exposures to toxins with only compromised protection for the sensitive brain.  A feeling of pain often has little or no relation to the actual condition of the body part where pain is sensed,14a and it therefore might result from a damaged brain.

 Fig. 9


Also, elevated levels of PCBs at age 4 were found to be linked, in a dose-response relationship, with reduced activity levels of children (see chart).15  That is significant here because exercise is recommended (including by the Mayo Clinic and Harvard Health) for dealing with depression16 and back pain.17  If early exposures to PCBs were to have resulted in low levels of activity, that could mean that effective natural means of reducing depression and pain would be less likely to succeed; that in turn could lead to feelings of despair and to resulting use (and possibly misuse) of drugs.



Back and/or joint pain are serious for many, and can be related to PCB exposures as follows: 

   (a) Healthy cartilage protects lumbar nerves from painful pinching and bones from painful rubbing by other bones;  

   (b) cartilage cells have been found experimentally to die following PCB exposure, in a dose-dependent manner;17a  

   (c) a group accidentally exposed to PCBs was found to have four times the arthritis of unexposed subjects; other studies found similarly.17a



Section 7:  Dioxins, strongly linked with liver disease, also increased in the environment during a period that would have been relevant to the increased mortality that was reported by Case and Deaton:


Another finding of Case and Deaton was increase in liver disease among most of the population but not among older people; the beginning of the increases of health problems in various areas, including liver disease, is said by these authors to be among Americans born in the 1940's.17b  This could be at least partly explainable by the recognized liver-damaging effects of dioxins, a chemical relative of PCBs that became significant in the environment after 1940.19,21  People born in 1940 and later would have been affected during their vulnerable developmental years, unlike the older group that would have had very little developmental exposure.  Special vulnerability to toxins during early development, with long-term consequences, was discussed earlier in Section 2;  to that should be added some text specifically on the subject of dioxins, in which the EPA refers to "developmental toxicity based on the inherent sensitivity of the developing organism;"21a the EPA says that this is supported by many different kinds of scientific observations.


Increases in exposures to dioxins would have been especially great in the years following World War II (after 1945), because


  -- burning of vinyl chloride plastics is known to the EPA to emit dioxins;26

  -- production of plastics (especially in consumer goods) expanded "explosively" after World War II;22

  -- shortly after that, there almost certainly would have been considerable trash consisting of disposable vinyl chloride plastic products, including toys and packaging23 to be disposed of; much of that would have been burned in municipal waste incinerators, hospital waste incinerators, and in backyard burning (the latter is common in rural areas)all of those are known to the EPA to emit large amounts of dioxins.23a  Efforts to reduce dioxin emissions from municipal and hospital waste incineration in the late 1900's were rather successful, but backyard burning continues to be widespread and a very major source of dioxin emissions.23a 


  -- During the 1950's, many more companies started to produce PVC plastics, and volumes increased dramatically during that decade.25



Recognized effects of dioxins related to pain, liver disease, cancer, lack of immunity, and mortality:


According to a report produced by the UK Department of the Environment, dioxin-like compounds elicit a broad spectrum of responses in experimental animals, with the first two on their list being liver damage and suppression of the immune system.  In fifth place on their list is developmental toxicity, followed by the explanation that "newborn offspring of several species have been shown to be particularly sensitive."27  The International Agency for Research on Cancer (IARC)29 and the National Toxicology Program have classified dioxin as a known human carcinogen.  According to Public Health England, reported effects of dioxins include not merely liver disease but "increased mortality from liver disease;" this agency refers to "low dose exposure" to dioxins as having been shown to cause tumors at multiple sites in rats and mice, including the liver.30  In 1991, the U.S. National Institute of Occupational Health and Safety reported its cancer mortality study of US workers exposed to dioxin, and found that mortality was increased from all cancers combined, particularly among those with the longest occupational exposure and the greatest latency from exposure.30g


Section 8:  Exposures during sensitive development leading to permanent alterations of systems, effects that may only be apparent at maturity: 

Reiterating a well-established finding, Public Health England also states, "developmental toxicity is the most sensitive toxic effect of TCDD (dioxin) observed in animal studies."30  Similarly, a publication of the U.S. National Academies Press states that some systems "may demonstrate particular sensitivity during the postnatal period."  That publication also refers to "specific periods in development when toxicity can permanently alter the function of a system at maturity...;" and also, "if a compound's toxicity is age related in one species, it is reasonable to assume that there will be an age relationship in other species in which the compound is toxic."1g 


The "age related" effects referred to just above obviously include effects of toxic exposures received during development that can permanently alter a system's function at maturity; and the "other species" referred to in the NAP publication, to which such age-related effects are relevant, are clearly intended to include homo sapiens.


The U.S. ATSDR agrees with all of the above, including the points that young animals are much more sensitive than adults to most of the immunological responses (p. 165).  Referring to dioxin's immune and developmental effects, the Agency states (p. 12), "It is reasonable to assume that these will also be the most sensitive effects in humans."24 


Latency of effects, especially related to cancer:  The ATSDR also says that  "damage may not be evident until a later stage of development." (p. 313)  The Agency mentions cancer as one example of long-term damage that can result from chemical exposures, damage that may not yet be observable during a significant part of the lifetime following exposure; but, at least in its report on dioxins, the ATSDR apparently considers extended latency also to be a characteristic of other diseases linked with toxic exposures, as well.


Along the lines of decades-long latencies of effects of dioxins, the following study is of interest.  In a mortality study of 5,498 workers in the United Kingdom employed in vinyl chloride manufacturing during 1940-1974 and followed through to December 1984, there were seven cases of primary liver tumors observed, as compared with 0.38 that would have been expected based on the number of workers, among autoclave workers.  (An autoclave is a heated container used for chemical reactions and other processes.)  The median latency was 25 years from date of first exposure to this work.30a  The authors of the study did not specifically refer to dioxins as a suspected causal agent, but there are good reasons to suspect dioxins as being the underlying cause of the major surplus of liver-cancer-related deaths, as follows:

  -- Dioxins are emitted during the vinyl chloride/PVC manufacturing processes;23a,23b

  -- dioxins have been determined by the IARC to be a known carcinogen;29

  -- dioxins are recognized to have adverse effects especially on the liver; (details in Section 7)

  -- the workers who were the ones with very unexpectedly high mortality were autoclave workers, who would have had especially close exposure to the chemical reactions that were probably the major source of the dioxin emissions.


To summarize the key point from the above:  There are good reasons to see early exposures to dioxins as being underlying causes of serious outcomes that appear decades after the exposures, especially outcomes related to the liver.


In another study, early gall bladder removal (which was thought to lead to inflammation in surrounding liver tissue) was found to be associated with doubled risk of liver cancer after 30 to 43 years, with the risk increasing with longer follow-up.  There was no association during the first 10 years after exposure.30b  So early minor harm to the liver might develop into substantial harm after a latency of several decades.  Remember that harm to the liver and developmental harm have been determined to be among the most prominent effects of dioxin exposure. (see above)


The above two studies dealt with liver cancer, as opposed to alcoholic liver disease and cirrhosis mortality, which Case and Deaton found to be increasing among U.S. whites. (p. 15 of Case and Deaton 2017)1d  But there is reason to think that there could be confusion between the above two categories, in reported data:

  --  according to the American Cancer Society, "It is often hard to find liver cancer early because signs and symptoms often do not appear until it is in its later stages;" and, unless a tumor is quite large, it would be "hard to detect on a physical exam because most of the liver is covered by the right rib cage." 30d

  -- also according to the American Cancer Society, "Many of the signs and symptoms of liver cancer can also be caused by other conditions, including other liver problems."30c 


Given the similarities of the symptoms, it would seem that diagnoses of other conditions might actually result from liver cancer, even when liver cancer is sufficiently advanced to produce observable signs and symptoms; that should be especially true since liver cancer is difficult to detect.


The test for liver cancer that the American Cancer Society discusses (other than ultra-sound) is the AFP test, which is said to be very imperfect;30d combining AFP with ultra-sound testing has been estimated (in a 2016 study) to cost $36,000 per early-stage tumor detected.30f  So cost of detecting liver cancer, combined with expected cost of treatment if cancer should be diagnosed, would lead to many people simply not undergoing the procedures for detecting the disease, even though it may well be present.  Therefore much of the mortality that is attributed in the Case and Deaton data to alcoholic liver disease and cirrhosis may actually result from undiagnosed liver cancer.


Regardless of which category is chosen to go into the death records, people would be likely to have been dealing with the symptoms by taking (pain-relieving) opioids or by consumption of alcohol.  


The financial constraints that limit diagnoses of liver cancer would apply especially to those without a BA degree, the group whose liver-related mortality has increased greatly, as reported by Case and Deaton (2017).1d 


So liver cancer may very well underlie much or  most of the drug-related and "alcoholic liver disease and cirrhosis" mortality that has been reported by Case and Deaton; lack of report of liver cancer may be simply that:  lack of reporting of a disease that may actually have been closely involved in the mortality, but which was often not reported because diagnoses have not been sought and/or because symptoms of liver cancer may have been (reasonably but incorrectly) attributed to other liver problems.  And in any case, even if the symptoms that led to a reported cause of death actually were effects of non-cancer problems, those other problems (drug use and alcoholic liver disease and cirrhosis) very likely resulted from something else:  the person's seeking relief from pain and ill feelings that stemmed from slowly-developing liver cancer. (Pain is one of the symptoms of liver cancer.30e)


Therefore the well-known latency of cancer could help explain the lag between greatly increased early-life exposures to dioxins (which began in the 1940's) and the increasing mortality decades later, in the affected age groups.  But remember from earlier that the ATSDR considers cancer to be only the most prominent among various diseases that have long latent periods.


Safe cancer-related dose, versus common actual dose:  The above discussion obviously provides no certainty that long-term harm caused by infant exposures to dioxins underlies the drug- and liver-related mortality increases reported by Case and Deaton; but there is good reason to consider that to be a strong possibility.  As will be dealt with in more detail in Section 9, the EPA has determined that a safe dose for exposure to dioxins for cancer-related effects is 0.006 TEQ/kg-day.39  That should be compared with the body-weight-based dose received by an apparently typical breastfeeding U.S. infant at initiation of nursing, as found in a 2002 study headed by an EPA senior scientist:  242 pg TEQ/kg-day.37a It should not be necessary to figure the precise ratio between the above two numbers, since it should be apparent from these numbers that many infant exposures to dioxins have been well within a high-risk range for cancer effects.  Also remember from earlier that liver damage is first on a list of many possible effects of exposures to dioxins, as presented in a discussion of animal test results by the UK Department of the Environment, along with the observation that "newborn offspring of several species have been shown to be particularly sensitive." 


So it would be easy when filling out death certificates to write down the immediate cause of death -- drug- or alcohol-related liver problems -- while not mentioning what may well have been the underlying causes of the drug and/or alcohol consumption:  pain and ill feelings resulting from slowly-developing, undiagnosed liver cancer.  In addition, information on death certificates has been seen to be of questionable accuracy; Case and Deaton (2017, p. 19)1d say that the authors of a 2017 study "argue persuasively that deaths attributable to diabetes are understated in the US, perhaps by a factor of four."  If it is credible that diabetes could be so far understated as a cause of death, it should also be credible that liver cancer, being slow to develop and difficult to diagnose, could be greatly understated as a cause of death; that is especially true considering that children are commonly exposed to a known carcinogen and cause of liver damage in doses that vastly exceed the established safe level. (see above)



Adverse effects, including on liver and immune function, repeatedly found to be linked with human infant exposures to dioxins at general background levels: 


The ATSDR notes (p. 345) that "several human studies have found significant alterations in markers of liver, thyroid, immune, and neurological function in young breast-fed infants of mothers with higher current background or general population CDD (dioxin) levels."24  So it seems to be well documented, on the basis of several human studies, that there are significant signs of effects on liver function in many infants who have received elevated exposures to dioxins at levels that are common in current times.  Also remember from Section 2 that early childhood is a period of especially great vulnerability to effects of toxins.


Especially great exposures to dioxins are common during infancy: 

According to the estimates in a 1999 study by a team of seven Dutch researchers, "The daily TEQ  (dioxin toxic equivalency) intake per kilogram body weight for infants breast-fed for 6 months is approximately 50 times higher than for adults, which was about the same as reported by the U.S. EPA."24a  However, the authors added that cumulative intake would not translate directly to body burden; body burden would be comparatively far less, as indicated in a study with monkeys described by the ATSDR in which, at weaning (4 months), the offspring had concentrations of dioxin in their sampled body fat 4.3 times higher than the concentrations in the sampled fat from their mothers. (p. 209 of ref. 24)



Far higher effects of dioxins, including pain and liver damage, when combined with exposures to PCBs, a combination that would occur frequently:  Dioxins can apparently have especially serious effects when combined with exposure to PCBs, to which developing children would often also have been exposed during a period relevant to the recent midlife health downturns (see PCBs in Section 1).  A dose of PCB that alone will cause a 1.5 times increase in hepatic (liver) porphyrins has been found, in the presence of dioxin at a dose that alone produces no measurable effect, to result in a 650-fold porphyrin increase.31  According to the Mayo Clinic, high levels of porphyrins can lead to various problems including severe abdominal pain, pain in the chest, legs or back, muscle pain, and mental changes such as anxiety and confusion.32  Excess porphyrins accumulate primarily in the liver33 and are associated with nerve damage and liver disease.34 


Long-term effects of dioxins:  Remember from earlier the statements from the ATSDR and two UK health-related agencies about special vulnerability to dioxins during development, including indication that effects of early childhood exposures might become evident only in later life.  This could result not only from latency of effects but also from the recognized persistence in the body of dioxins; in a 2011 study (by Mocarelli and 12 others)34a  the following was found:  even at ages 18 to 26, average dioxin concentrations were still twice as high in young men who had had higher concentrations during infancy (those who had been breastfed) as in those who had not been breastfed; this relationship was found in each of two separate groups that were studied.34b  Continuing elevated levels of dioxins in adulthood (resulting from exposures in infancy), with likely continued effects of reducing immunity, could very well result in adverse outcomes that become apparent only in midlife. 


Remember from earlier that reduced immunity is known to result from exposures to dioxins; this could lead to increased later susceptibility to various diseases, including diseases for which those in midlife may be especially at risk, including diseases linked with smoking, obesity, and occupational exposures.  Also, effects such as liver damage might be unnoticed for many years due to their internal location (covered by the rib cage),30d but could leave the liver with increased vulnerability to effects of later alcohol consumption. Higher activity levels during youth could also help to conceal for many years effects that might be developing from low-level disease. (See Figure 9 and accompanying text about pain-reducing effects of activity.)  Also remember from earlier the discussion of latency especially in relation to liver cancer.


Therefore, for many reasons, a serious inquiry into origins of increases in pain, liver disease, and mortality really ought to include examination of exposures to dioxins; that is especially true regarding any increases in exposures that would have taken place during the vulnerable developmental periods (see Section 2) of those who later, in midlife, would have the health problems reported by Case and Deaton. Remember (from early in Section 7) the probable rapid increases of dioxins in the environment after 1940 and especially after World War II, which could have led to rapid increases in the diseases and mortality in midlife as reported by Case and Deaton; people born in earlier years would not have had those dioxin exposures during their vulnerable developmental periods, very likely explaining why older people were not affected by the health declines.



Section 9:  Safe exposures to dioxins that have been determined, versus actual exposures that many developing children receive:  


There is good reason to believe that exposures to dioxins could have been high enough to lead to the health declines that have been reported by Case and Deaton.  The reasonably-safe upper thresholds of daily exposure (RfDs) to dioxins have been determined to be

  --  1 pg TEQ/kg-day (picograms of dioxin toxic equivalency per kilogram of body weight per day), as estimated by the ATSDR,37b 

  --  0.7 pg TEQ/kg-day for non-cancer effects, as estimated by the EPA,37 and

  --  0.006 TEQ/kg-day for cancer-related effects, as estimated by the EPA.39



Those figures should be compared with the far higher body-weight-based dose received by an apparently typical breastfeeding U.S. infant at initiation of nursing, as found in a 2002 study headed by an EPA senior scientist:  242 pg TEQ/kg-day.37a  In a 1999 Dutch study, infants breastfed for six months were estimated to receive on average about 115 pg TEQ/kg-day;38 this is compatible with 242 pg at initiation, since concentrations of dioxins in breast milk are known to decline with duration of nursing, and since there will inevitably be local variations in the pollutants that accumulate in the body.



Section 10:  Probable locations of especially high exposures to dioxins make a good fit with the geographic distribution of the increased health problems reported by Case and Deaton:


Case and Deaton found high midlife health problems in the U.S. but much less in comparison countries, and they found less such problems in large cities than in rural areas.  There are good reasons to believe that open burning  of plastics-containing trash, a common practice in the rural U.S. but apparently not in most of the comparison countries, has been of major importance in producing dioxins that may have been substantial causes of the health declines described by Case and Deaton.  Such burning would have begun on a large scale after plastics came into the waste stream during the 1940's (see beginning of Section 7); that would have resulted in exposures of children to dioxins, during their vulnerable developmental periods, exposures that could have resulted in increased disease and mortality that were only well-noticed much later in the children's lives.  Details will follow.


The following is according to the EPA:  Current theory proposes that dioxins are formed within the cool-down region of combustion processes, when carbon, oxygen and chlorine are all present.  "Chlorine sources present in feeds are necessary for dioxin formation...."  Experimental evidence suggests that combustion of PVC (polyvinyl chloride in plastics, incorporating chlorine) generates substances that may contribute to dioxin formation.40


Open burning of trash (which would typically contain PVC plastics), often referred to as backyard burning or backyard barrel burning, is common in rural U.S.; also common is the practice on U.S. farms of burning the large plastic wraps that cover hay bales.41  And such burning is known to the EPA to be a major source of dioxin emissions -- the largest quantifiable source of dioxin emissions in the U.S. as of the latest national inventory.23a  Compared with combustion in large, professionally-built incinerators, open burning typically takes place largely in the lower end of the temperature range, where dioxins are most readily formed.  As indicated in a study published by the EPA (see chart below, noting that PCDDs and PCDFs are dioxins), dioxin emissions from just a few open-burning households could equal the emissions from a municipal waste combustion facility that burns 200 tons of waste per day.

Fig. 10

Source of this chart:  EPA/ NSCEP document referenced at 43


But the quantity of emissions from household and farm open burning is only part of the problem.  Emissions from municipal incinerators come out of stacks, keep rising for some distance because of their high temperatures, and become very diluted by wide dispersion.  That compares with, as stated in the above study, "the concentration of these emissions in the local neighborhoods due to poor dispersions..."  Concentration of the dioxin emissions in local neighborhoods would apply especially in valleys, where towns are often located.  Another EPA web page states, along similar lines, "Backyard burning is particularly dangerous because it releases pollutants at ground level where they are more readily inhaled or incorporated into the food chain."45



Section 11:  Summary of what appears to have happened in the U.S., relating that to the time of the upturn in adverse health outcomes, and seeing how that relates to what has not occurred in the comparison countries:


Remember from earlier that many developing children receive exposures to dioxins that vastly exceed established safe levels, receiving these exposures during a particularly vulnerable period of their lives.  And these exposures greatly increased at a time (late 1940's) that is compatible with the reported later adverse outcomes; those later outcomes could have resulted from

   a) lack of immunity, which is a recognized effect of dioxins (see earlier) with obvious long-term consequences when occupational and other toxic exposures are encountered in adulthood, or from     

   b) liver cancer, another recognized effect of dioxins with consequences typically becoming apparent only over the long term;


and, following decades of latency, the adverse outcomes could have become noticeable in those people in midlife, during the most recent decades.


                   Time of the upturn in mortality in the U.S.:

    Fig. 11

image016.gifIn this chart from Case and Deaton (2017),1d it is hard to miss the unfavorable upturn that took place in all-cause mortality among American whites ages 45-54 after 1997, in contrast with the continued declines in mortality in all of the comparison countries.  Bearing in mind the effects of dioxin exposures that take place during early child development, including reduced immunity, we should review what was taking place 50 years before the adverse turn shown:


Production of plastics increased dramatically after the end of World War II (1945), which would soon have led to considerable plastics waste to be disposed of, which in turn would have led to much open burning (at least in the U.S.) of a kind that is known to release large amounts of dioxins in close proximity to many people.  Allowing for a lag after production of the disposable plastics before they would end up in backyard burning, leading to people being  exposed to the resulting dioxin emissions, 1947 is about when one would expect a major upturn in early developmental exposures of children to dioxins. 


As will be discussed below, this type of burning appears to have been common practice or to have produced harmful concentrations of dioxins predominantly in the U.S.


What was happening in comparison countries in this area:  It is revealing to look at the data for the other countries used for comparison in Case and Deaton (2017),1d Table 2.  The three countries that were next highest in the drugs, alcohol and suicide category of mortality increases (behind only the U.S. in this long list) were Ireland, Canada and Australia.  In that regard, note that, in a substantial online search for articles about backyard burning of trash, those three were the only countries among the 13 comparison countries where this kind of burning was reported to take place.46


A publication of a European plastics industry organization would not ordinarily be considered as a good source for data such as this, but considering the lack of published information about backyard burning in Europe, some observations from such a publication may be helpful.   The author refers to "backyard burning of household trash, a widespread practice in the developing world and rural parts of the U.S.," while saying nothing about such activity in Europe.44 Talking about a practice as being widespread in the U.S. and certain other countries while saying nothing about its presence in one's own region would be unlikely in such a publication unless there actually did exist a major difference between the two areas in prevalence of the activity being discussed.  



Backyard burning no doubt does take place in some European countries other than Ireland and Romania, but (possibly because of population density), it apparently is not common in European countries.  In the two non-European comparison countries (Australia and Canada), population density is so low (four per square kilometer and less in the data most relevant to this discussion)44a that exposures of nearby people to emissions from open burning would probably be minimal compared with such exposures in the U.S.  However, even though mortality outcomes in Ireland, Australia and Canada were less unfavorable than in the U.S., those outcomes were worse in all of the four countries in which backyard burning is reported to occur than in any of the 10 countries regarding which there was no mention of backyard burning (Table 2 at 1d)


One might wonder what the odds would be of the following (discussed above) being a chance occurrence:

 --- There appear to be very few countries in the entire developed world where backyard burning is of sufficient concern for it to be reported about in an article that comes up in an online search;

  --- in a ranking of 14 countries according to drug, alcohol and suicide mortality increases, all four of the countries with the largest mortality increases came from that small group in which backyard burning is common.


There appears to be no question that this type of burning produces dioxins in large amounts, and little reason to doubt that many people are hazardously exposed to those major emissions specifically as a result of that type of burning. (see above)  And developing children are frequently exposed to dioxins in doses far exceeding authoritatively established safe doses (see earlier), at a stage of their lives that is known to be especially vulnerable to effects of such toxins. (see Section 2)  Remember from Figure 11 and accompanying text that all-cause mortality among white Americans aged 45-54 increased dramatically at a time that was very compatible with the rapid entry of plastics (important for creating dioxins) into the waste stream at a very relevant time:  when those plastics would become part of backyard burning during the vulnerable infancies of those with increasing mortality.



To bring together a key point, from earlier:  There is good reason to believe that high dioxin emissions (from backyard burning) closely affecting nearby people would not occur nearly as widely or be nearly as concentrated in the comparison countries as is the case in the U.S.; this may  explain why the increases in health problems and mortality (as reported by Case and Deaton) have been much higher in the U.S. than in those other countries



Section 12:  Ethnic differences in mortality increases:  Case and Deaton point to the fact that the health declines in the U.S. were distinctly high among non-Hispanic whites, while African-Americans and Hispanics had little or none of such trends.  In that regard, we should remember that backyard burning is a predominantly rural practice, and then note that U.S. farmers are very disproportionately white.  The U.S. Department of Agriculture states that only 3% of U.S. farmers were Hispanic in 2012,47 whereas 16% of the U.S. population was Hispanic at about that time.48  The USDA also reports that only 1.4% of all U.S. farmers are black,49 whereas 13.3% of the U.S. population are black or African-American;50 and also that 93% of U.S. farmer operators in 1982 were white men, as well as an additional few percent who were white women,50a whereas only 83% of the population was white in 1980.50b 


To sum up:

--  black representation among farmers is about a tenth of what would be expected based on their percentage in the U.S. population,

-- Hispanic representation among farmers is about a fifth of what would be expected based on their percentage in the U.S. population, and

-- White representation among farmers is much higher than would be expected based on whites' percentage in the U.S. population,


So, if there is an exposure to toxins that is known to be especially common in rural areas (such as dioxins from backyard burning), possible adverse health effects of that exposure would be expected to be comparatively

-- high among whites,

-- very low among blacks, and

-- low among Hispanics, but much higher than among blacks.


And that is exactly what the relative increases in drug, alcohol and suicide mortality were like among those ethnic groups as recorded in Table 2 of Case and Deaton (2017) 1d

-- high among whites (0.054)

-- very low among black non-Hispanics (0.001), and

-- low among Hispanics, but much higher than among blacks (0.010).


An outcome such as the above, with a distinctly unfavorable trend being apparent only for the (generally-better-off) whites, seems surprising; it is especially noteworthy since the markedly adverse trend just for U.S. whites continued over a period of decades (see Figure 2); so this would seem to call for a rational explanation.  The following would seem to be such an explanation:


First note that, when Case and Deaton refer to "alcohol" (in "alcohol mortality," as said within Figure 1.5 in Case and Deaton 2017),1d that appears to be their shorter way of saying "alcoholic liver disease and cirrhosis" mortality, as it is expressed when they say it more fully in the text next to that figure; so the disease that is increasing is very much related to the liver.


Then, to try to understand the adverse outcomes predominantly among whites, note the following:

   -- dioxins are recognized to be developmental toxins, with especially harmful effects on the liver (see earlier);

   -- many people are exposed, during sensitive, vulnerable periods of development (see earlier) to dioxins at levels that far exceed authoritatively-established safe levels (see earlier).

   -- backyard burning is known to the EPA to be a major source of dioxin emissions, and it is a source to which people are exposed in " particularly dangerous" concentrations (see earlier);

   -- remember from above that backyard burning is basically a rural practice, and that U.S. farmers are very disproportionately white, the ethnic group that is reported by Case and Deaton to have by far the worst trends for liver-related mortality.


So we see

   (A) large differences in ethnicities represented among U.S. farmers,

   (B) ethnic differences in mortality that could well result from dioxins to which rural people are distinctly exposed, and

   (C) the ethnic differences in mortality align very well with the ethnic differences in exposures to dioxins on typical farms


So the ethnic differences in mortality could be seen to be a logical consequence of major differences in ethnicities represented among U.S. farmers.


But couldn't the mortality differences result from farmers' greater exposures to pesticides?  Not necessarily.  According to a 2011 California study (Weldon et al.), investigating pesticides in breast milk samples from the urban Bay Area and a rural area, detection rates of chemicals (including pesticides) for urban populations were similar to those for agricultural populations.  The authors attributed the urban exposures mainly to pesticides in foods.51  So the farmer-versus-urban differences in pesticide exposures would seem to be not nearly large enough to account for ethnic differences in mortality as large as the ones found by Case and Deaton.  The far greater exposures of (disproportionately white) farmers and their children to dioxins from backyard burning, compared with minimal exposures of blacks and Hispanics, could be a better explanation for higher mortality among whites.


Section 13:  Dioxin and PCB exposures as related to urban versus rural exposures, in parallel with health declines:

Bear in mind the substantial evidence indicating that harm to health observed in the early 2000's could well be linked with children's developmental exposures that took place in earlier decades (as presented earlier); then notice that Case and Deaton found that mortality increased on average 1 per cent per year in the four smallest of six urban-versus-rural residential classifications according to size, did not increase in the second-from-largest category, and actually fell in the largest metropolitan category. (p. 21 of Case and Deaton 2017) 1d  That might bring up the question as to whether there could be some benefit, related to this recent mortality trend, in residing in areas with high population density.  It turns out that there is considerable reason to suggest the existence of such a benefit, with good biological evidence explaining why it should be that way.


Figure 1.9 from Case and Deaton (2017) 1d, shown below, depicts the most recent mortality data for the demographic category as indicated in its title, showing areas with higher mortality rates as darker areas..

Fig. 12



The geographic pattern shown above bears at least a passing resemblance to a representation of U.S. climate zones as defined by U.S. NOAA and depicted by the U.S. Energy Administration.  See below.

Fig. 13




Possible reasons for the apparent geographic relationship between mortality differences and climate zones will be discussed later, in Section 14.  


For now, we will discuss some of the details in the mortality data that merit closer looks for possible causes other than climate effects. A close examination of the Case and Deaton map in Figure 12 above shows that local areas of lower mortality are normally areas of high population density:  cities or groups of cities.  So an initial look at a map from the U.S. Census Bureau (below) depicting population density might be helpful.

 Fig. 14




The above map shows high population density conspicuously in two large areas where, as shown above in Figure 12, mortality is unusually low:  in the Southwest coastal area and in the I-95 corridor in the Northeast.  In addition, a closer look at an enlargement of the Case-Deaton mortality map (below) shows that the great majority of the smaller areas shown above with high population density -- and marked with blue below -- also have low mortality.  These higher-density/lower-mortality areas are also indicated below by names of cities at those same locations.


Fig. 15




image021.gifSo there appears to be fairly consistent correlation between greater population density and lower areas of mortality, within a region.


In some cases, the map above does not show zones in sufficient detail for certain metropolitan areas to show up well, as in the cases of Boise (Idaho), Billings (Montana), and Denver (Colorado) above.  But a different map showing mortality data within the relevant period, such as the one for the year 2000 on the left, might provide sufficient detail to allow the normal higher-density/lower-mortality relationship to be observable.


So there is good reason to think about a possible beneficial effect associated with high population density, or (seeing the same outcomes from a different angle), a harmful effect associated with low population density.  Harm connected with low population density, as long as some humans are present, can reasonably be postulated as follows:

   a) Backyard burning, recognized to emit dioxins in a way that causes people to be closely exposed (see earlier), is distinctive to rural areas in the U.S.; an urban-rural divide such as this has been well reported and is also as would be expected for reasons such as numbers of people who might be bothered or harmed by neighbors' burning;55


   b) those rural exposures to dioxins are hazardous to health, especially exposures that take place during infancy (see Section 9), a stage of development when long-term health can be endangered by toxic exposures (see Section 2);


   c) emissions of dioxins by this kind of burning would have rapidly increased at a time that seems to be very compatible with the timing of the mortality increases that have been reported by Case and Deaton; production and distribution of disposable plastic products increased dramatically after World War II ended (1945), which would soon have resulted in considerable dioxin-emitting burning of plastics in rural backyards. (see Figure 11 and accompanying text)   And, as reported in Case and Deaton (2017, p. 171d), it was "after the 1945 cohort" that mortality rose in each birth cohort for all three causes of death.  Those born in the earlier cohorts, by contrast, would have already passed their especially sensitive early developmental periods by the time dioxin emissions increased greatly; and those people have not been affected by the increasing mortality that has been found in later cohorts.


So it should not be surprising that, when Case and Deaton reported about comparative mortality rates among six different size classifications on a scale from rural to large metropolitan (see beginning of Section 13), the largest metropolitan category had the most favorable results and the second largest metropolitan areas had the second most favorable results.  Three smaller urban classifications had mortality increases that were similar to that in rural areas, which may be related to the following:

   a) emissions from backyard burning taking place around the fringes of a city would drift far enough to reach a larger percentage of the population if the city is small;

   b) industries that emit dioxins and other pollutants would probably normally want to locate plants near population centers that are large enough to be able to provide a satisfactory pool of potential workers, but no larger than would be necessary for that purpose, in order to minimize the number of neighboring people who would object to the pollution.  Polluters could expect friendlier treatment by local authorities in locations where they are an important part of the local economy, compared with larger cities where bothered neighbors would be more numerous and where the loss of a significant employer from the area would be politically acceptable.


Section 14:  Harmful exposures related to climate  differences:

Remember from Figures 12 and 13 above (shown again below, reduced) that there appears to be a general similarity between the geographic pattern of mortality and that of climate zones in the U.S.

Review of Figures 12 and 13



Although the relationship of climate zones to mortality is only very approximate, it should give us something to think about.  One likely source of a climate-mortality relationship has to do with exposures to dioxins on average being greater in warmer areas, as indicated by the following:

--  (As explained by the U.S. ATSDR):  At cooler temperatures, dioxins are likely to be removed from the air by deposition, since they become attached to particulates at cooler temperatures, and the particulates can then be removed from the air by deposition; at warmer temperatures, on the other hand, dioxins are likely to present in the vapor phase, a form that is not likely to be removed from the air by deposition.52  Also, higher temperatures generally increase volatilization of dioxins.53

--  The above generalizations were not quantified, but there may well be relevance in what has been found with regard to volatilization of PCBs, to which dioxins are recognized to be similar in various ways:56  As indicated earlier, according to a study referred to in an EPA document, the PCB emission rate from solid form was found to increase 400-fold as the temperature increased from 30 to 50 degrees C (86 to 122 degrees F).8f 

--  Aside from climate's effect on airborne dioxins, another way in which it would affect mortality would be as a result of the effect of heat in increasing PCB emissions, as just  mentioned.  Remember from Section 1 that PCBs are ranked by the ATSDR as being among the top five priority hazardous substances,1c and from Sections 2 and 5 remember that developmental exposures to PCBs are toxic to immunity and to the blood brain barrier; both of the latter effects would be expected to cause long-term harm to infants born in the late 1940's and later, when exposures to PCBs increased greatly and close to the time when dioxin exposures increased substantially.


People may think that there is little reason to be concerned about airborne dioxins, since it is often said that 90% of typical human exposure to dioxin is via food.  But that generalization is almost certainly based on studies carried out where atmospheric exposures are not especially high (research groups are relatively unlikely to be located in rural areas).  In the NHANES 2003-2004 survey, people with well-above-average dioxin levels (the 95th percentile) averaged 5.2 picograms/gram (pg/g) of lipid; on the other hand, dioxin levels in chemical plant workers with higher exposures have ranged as high as 2,000 pg/g lipid.54  One can be confident that lipid dioxin levels hundreds of times higher than normal would not have resulted mainly from exposure via food, among those chemical plant workers.  Remember from earlier the discussion about the concentrations of dioxins emitted by backyard burning, and consider whether the concentrations from backyard burning might be similar to those inhaled by the chemical plant workers


As further evidence of the seriousness of rural exposures to dioxins, note the following from an EPA document:  Atmospheric concentrations of dioxins in rural areas where crops and livestock were grown were found to be 6.4 fg/cu near the low end (95th confidence interval), as compared with the equivalent reading of  0.1 in remote areas.55  And that 6.4 low-end measurement from farming areas was almost certainly not taken near actively-burning trash.


Section 15:  Differences in mortality according to education:


Case and Deaton (2017, p. 81d) point out that increasing midlife white mortality rates are particularly high for those with no more than a high school degree.  Near the end of the previous section we saw one reason why such differences should exist:  workers in chemical plants have been found to have very high levels of dioxins; those workers would be relatively unlikely to be college graduates.  That would also apply to farmers, with their exposures to open burning; U.S. farmers are well below half as likely to be college graduates, as compared with the general population.57  Occupational categories indicated by the ATSDR to have exposure to dioxins include fire fighters, cleanup workers involved with transformers, and workers involved in incineration operations, metal reclamation facilities, and producing and handling pesticides and a variety of other chemicals. (Section 5.5.2 of ref. 21So it should be apparent that many workers would have occupational exposures to dioxins, and very few of those workers would be college graduates.  Also see Section 5 about probable low representation of college graduates in the trades that would have had greatest exposures to PCBs, effects of which would be in addition to the mortality effects of dioxins, beginning at very much the same time (late 1940's) when exposures to dioxins increased greatly.


Aside from exposures of people working within industrial facilities where dioxins and PCBs are emitted, people who live around those plants, exposed to the emissions, would also be relatively unlikely to be college graduates; the degree holders would typically live farther away in suburbs, better removed from the pollution.  That could especially affect their children during critical stages of development.  Working-class children would also be exposed to chemicals brought home on skin and clothing by parents employed in the industries.1b


Section 16:  Other health declines, including sciatica:  Adverse health effects of dioxins have been found to include bone toxicity,30g particularly during development.30h (more on this below)  That, combined with effects of PCBs in damaging cartilage,17a could help explain the increases in sciatica among those with less than a BA, as have been reported by Case and Deaton (2017, Figure 1.131d).  (See Section 15 for reasons why those with less education would have greater exposure to dioxins, and Section 5 for reasons why those with less education would have greater exposures to PCBs.)


More evidence of bone toxicity of dioxins:  A 2010 study with rats found confirmation that developmental TCDD (dioxin) exposure has adverse effects on bone size, strength and mineralization;63 and another study found that dioxin exposure reduced bone strength in a dose-dependent manner, even though bone mineral density was not reduced; the strength reduction resulted from dioxin "exposure levels only slightly higher than the current average human exposure."69 (Bear in mind that many people will have dioxin exposures that are higher than average.)  A later Finnish study found that dioxin exposure of mice caused increased porosity in cortical  bone (the dense, hard, strength-giving outer layer of bone) of females. Bones of exposed females also showed reduced yield strengths. The author pointed out that "Reduced yield strength indicates increased microfracture susceptibility...," results that were said to generally "indicate early onset of skeletal senescence;"(p. 66) and later, dioxin exposure was said to lead to "increased porosity and brittleness of tissue."(p. 69)61  Developmental dioxin exposure has been found to harm bone development in monkeys also.64  So developmental dioxin exposure apparently leads to weaker, more porous bones, meaning greater risk of micro-fractures.


Although "micro" sounds very small, the pain resulting from micro-fractures can be very significant, at least if those fractures are in vertebrae.68


Micro-fractures recognized to occur in lower back:  Stress fractures in bones are one kind of micro-fracture.  A 2016 study referred to the lumbar area as one of seven parts of the body where stress fractures are likely to occur;62 that recognition is despite the fact that such fractures are very difficult to detect.65,66  The authors said that one result of such fractures was formation of bone calluses and other thickening.  Nerve roots in the lower back are tightly packed, exit from the spinal column through shallow lateral recesses, and may be compressed easily,70 and there is danger of painful pinching of the nerve if the opening becomes smaller; thickening and/or calluses at certain places in vertebrae, following micro-fractures, could well be a source of such pinching and resulting long-term lower back pain. 


Micro-fractures in vertebrae, resulting from back accidents and repeated stress, are associated with sciatica, and "repeated minor injuries (of the vertebrae) are presumed to cause irreversible damage and hasten the degenerative process in the spine."67


Given the above, remember that dioxin exposure has been found to be toxic to bone strength and to increase susceptibility to micro-fracture.


Section 17:  Mortality was found to be increasing faster in white non-Hispanic women than in white non-Hispanic men, according to Case and Deaton (2017, p. 8).1d  This, too, is explainable on the basis of dioxin exposures:

   a) Greater levels of dioxins have been found in women than in men, in separate studies in Japan and the U.S.59

   b) Animal testing has found dioxin to weaken bones specifically in females;61. in line with that, fatigue fractures in bone have been found to be more frequent in women than in men;66 the fractures are likely to be painful, leading to use (and possible fatal misuse) of painkillers.  

   c) First note that medical waste incineration in 2000 has been estimated by the EPA to contribute 27% of all quantifiable dioxin emissions in the U.S as of the year 2000 (behind only backyard burning, at 35%).23a  Then consider which sex would be disproportionately inhaling those medical waste incineration emissions; over 76% of U.S. hospital workers are women.60

   d)  Substantially greater cancer-related effects of dioxins have been found in females than in males:  According to a publication of the U.S. National Research Council, increases of cell proliferation in female rat livers, possibly leading to tumors, have been found 30 weeks after dioxin exposure; and it was reported that "The sensitivity of female rat liver to dioxin... clearly depends on ovarian hormones," citing two studies as evidence.  Also, "hepatotoxicity was less pronounced in male rats, for which no increase in tumors was seen. The hepatocarcinogenicity in female rats is related to estrogens."58






What is to be done?

Trying to prevent formation of dioxins during household burning by removing sources of chlorine (which is necessary for formation of dioxins) is ineffective since "...low levels of chlorine are present in most household trash."

EPA:  The Hidden Hazards of Backyard Burning, at




About the author:

My main qualification for writing the above is ability to find and pull together large amounts of scientific evidence from authoritative sources and to condense the most significant parts into a form that is reasonably understandable to the general public and also sufficiently accurate as to be useful to interested professionals. My educational background included challenging courses in biology and chemistry in which I did very well, but at least as important has been an ability to correctly summarize in plain English large amounts of scientific material.  I scored in the top one percent in standardized tests in high school, graduated cum laude from Oberlin College, and stood in the top third of my class at Harvard Business School.  


The reader is strongly encouraged to check the source(s) regarding anything he or she reads here that seems to be questionable, and to notify me of anything said in the text that does not seem to accurately represent what was said by the original source.  Write to  I will quickly correct anything found to be inaccurate.


For a more complete statement about the author and Pollution Action, please go to


Don Meulenberg

Pollution Action

Shenandoah, VA, USA





1) Project TENDR: Targeting Environmental Neuro-Developmental Risks The TENDR Consensus Statement, Environ Health Perspect. 2016 Jul; 124(7): A118–A122. at


1b) World Health Organization International Programme on Chemical Safety (IPCS) Document on:    Principles for Evaluating Health Risks In Children  Associated with Exposure to Chemicals, p. 157,  by a team of researchers including nine from the U.S. and others from Canada, Denmark and Mexico, at


1c) ATSDR's Substance Priority List, at

1d) Case and Deaton, Mortality and morbidity in the 21st century (Final post-conference version), May 2017, at


1e)  Polychlorinated Biphenyls and Polybrominated Biphenyls, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 107, IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, 2016,  Section 1.3.2, at


1f)  MacIntosh et al., Mitigation of building-related polychlorinated biphenyls in indoor air of a school, Environ Health. 2012; 11: 24, at


1g) Commission on Life Sciences, National Research Council:  Pesticides in the Diets of Infants and Children, p. 43, National Academies Press, Washington, D.C.  1993, at


2) WHO: Don’t pollute my future!  The Impact of The Environment on Children’s Health, pp. 22 and 11, at


2a) WHO: Summary of Principles for Evaluating Health Risks in Children Associated with Exposure to Chemicals, p. 20, at     Also see pp. 26 and 75 of the document at reference no. 5a:    Regarding one example of long latencies, the International Agency for Research on Cancer (IARC) has classified PCBs as carcinogenic to humans (Group 1) (see reference no. 13 below)


3) Grandjean et al., The Faroes Statement: Human Health Effects of Developmental Exposure to Chemicals in Our Environment, Basic and Clinical Pharmacology and Toxicology, Volume 102, Issue 2, February 2008 at


4) UMassAmherst, Environmental Health and Safety:  Polychlorinated Biphenyls (PCBs) - Hazardous Building Materials, at


4a) European Commission:  Science for Environment Policy:  Building materials used between 1950 and 1980 in Europe may contribute to PCB air pollution, 15 Apr. 2016, at

5) EPA:  Polychlorinated Biphenyls (PCBs) in Building Materials, at https://19january2017snapshot.epa.



5b) EPA:  PCBs in Building Materials -- Questions and Answers, July 28, 2015, p. 17 at https://www.epa.


6) USGS:  Field Manual of Wildlife Diseases: Birds, Ch. 41, p. 303, at

7)  Breivik et al., Towards a global historical emission inventory for selected PCB congeners — a mass balance approach: 1. Global production and consumption, Science of Total Environment, Vol. 377, Issues 2-3, May 2007


8) PCBs in the Environment, National Research Council, 2001. A Risk-Management Strategy for PCB-Contaminated Sediments. Washington, DC: The National Academies Press (p. 28 about spills), at


8a) State of Connecticut Department of Energy and Environmental Protection:  PCB Program document at   

    Also Texas Dept. of State Health Services document at, p. 3


8b) WHO: Air Quality Guidelines, 2nd Edition, 2000, Ch. 5.10: PCBs, at


8c) Residential Roofing Products Guide, Legends Roofing Co., at


8d)  The 3 Most Popular Roofing Materials in Australia, at

   See also web page at, indicating that asphalt shingles may be hard to find in Australia


8e) Barbour blog:  Pros & cons of popular roofing materials, Oct 2014  <at

    Also, Asphalt Shingles:  Why are they so popular? at


8f) p. 2 of EPA:  EPA/600/R-11/156 October 2011 Laboratory Study of Polychlorinated Biphenyl (PCB) Contamination and Mitigation in Buildings, at


8g) Oregon Department of Environmental Quality:  Fact Sheet: Sources of Polychlorinated Biphenyls, Table 2,



8h) The Local SE: Sweden's news in English, 3 July 2012: What's on your house?

Roofing question, at

8j) Government of Australia:  1999 National Environment Protection (Assessment of Site Contamination) Measure 1999, Schedule B7


9) Ahlborg et al., Risk Assessment of Polychlorinated Biphenyls (PCBs). Environmental Report in the Nord Series. Nord 26. Copenhagen: Nordic Council of Ministers, 1992, p. 36, at   "Behavioural/developmental disturbances (hyperactivity) in Rhesus monkey infants have been reported at doses of about 6 µg (0.006 mg) Aroclor 1248 per kg and day to the (gestating/lactating) mother." (p. 37) Assuming a recognized average weight of 5.3 kg (12 pounds) per female monkey, this works out to 0.032 mg per monkey per day, or a dose of less than one 100,000th of one ounce of Aroclor per day per gestating/lactating female monkey. 


10) Robertson and Hansen, Eds., PCBs: Recent Advances in Environmental Toxicology and Health Effects, Univ. Press of Kentucky, 2001, p. 18, at  


11) Derek Thompson, The 33 Whitest Jobs in America, The Atlantic, Nov 6, 2013 at


11a) Oregon Department of Environmental Quality Environmental Cleanup Program, Oct. 2010, 10-LQ-023, p. D2-4 (attachment 2 of Appendix D, near very end) at


11b) EPA:  Biomonitoring / Polychlorinated Biphenyls (PCBs):  America's Children and the Environment, 3rd Ed., at


11c) The Surgeon General’s Call to Action to Support Breastfeeding 2011,   U.S. Public Health Service, Table 2,  at,


12) World Bank data at

13) ATSDR web page on polychlorinated biphenyls PCBs) at

Also see p. 2 of EPA:  Laboratory Study of Polychlorinated Biphenyl (PCB) Contamination and Mitigation in Buildings, at


14) Seelbach et al., Polychlorinated Biphenyls Disrupt Blood–Brain Barrier Integrity and Promote Brain Metastasis Formation, Environ Health Perspect. 2010 Apr; 118(4): 479–484. Published online 2009 Oct 28.  At


14a) Mosely, Reconceptualising Pain According to Modern Pain Science, Body in  Mind, Oxford Centre for fMRI of the Brain, Oxford University, Oxford, UK, at journal-articles/full-text-articles/reconceptualising-pain-according-to-modern-pain-science.


15) Jacobson et al., Effects of Exposure to PCBs and Related Compounds on Growth and Activity in Children, Neurotoxicology and Teratology, 1990, Vol. 12, pp. 319-326, at


16) Mayo Clinic webpage on Depression and Anxiety, at

   Harvard Health Letter at


17)  Mayo Clinic webpage on Back exercises in 15 minutes a day, at   Harvard Health at edu/blog/heres-something-completely-different-for-low-back-pain-2017070611962


17a) Lee et al., PCB126 induces apoptosis of chondrocytes via ROS-dependent pathways, Osteoarthritis and Cartilage, Vol. 20, 2012, at

  Also Abella et al., Environmental pollutants and osteoarthritis: Effects of non-dioxin-like polychlorinated biphenyls on cultured chondrocytes, Osteoarthritis and Cartilage Vol. 22, Supplement, Apr 2014,



17b) Case and Deaton, Rising morbidity and mortality in midlife among white non-Hispanic Americans in the 21st century, PNAS, Dec. 8, 2015, vol. 112 no. 49, at;

   also p. 41 of Case and Deaton, Mortality and morbidity in the 21st century (Final post-conference version), May 2017, at


18) ATSDR:  Polychlorinated Biphenyls (PCBs) Toxicity: What Are Routes of Exposure for PCBs?  at


19) ATSDR: Polychlorinated Biphenyls (PCBs) Toxicity:  What Are Adverse Health Effects of PCB Exposure? at


20) U.S. Geological Survey, Field Manual of Wildlife Diseases: Birds: Ch. 41,  Polychlorinated Biphenyls, p. 304


  Also Rand Corp. document at

  Also Oregon Department of Environmental Quality, Fact Sheet: Sources of Polychlorinated Biphenyls, Table 2, at


21) ATSDR dioxin document, Toxicological Profile for Chlorinated Dibenzo-p-Dioxins, 1998, pp. 379 and 391, at


21a) EPA:  Dioxin: Scientific Highlights from the

NAS Review Draft of EPA’s Dioxin Reassessment, Information Sheet 2, p. 4


22) Freinkel:  A Brief History of Plastic's Conquest of the World, Scientific American,  at


23) Tox Town: Polyvinyl Chloride (PVC), at


23a)  EPA:  An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000, especially Table 1-17


23b) Ehrlich, The PVC Debate: A Fresh Look, at


24) ATSDR dioxin document, Toxicological Profile for Chlorinated Dibenzo-p-Dioxins, 1998, including pp. 153, 161, 163, and 165, at


24a) Patandin et al., Dietary exposure to polychlorinated biphenyls and dioxins from infancy until adulthood: A comparison between breast-feeding, toddler, and long-term exposure, Environ Health Perspect. 1999 Jan; 107(1): p. 50, at


25)  The history of PVC, at


26)  ATSDR:  Toxicological Profile for Chlorinated Dibenzo-P-Dioxins, p. 378, at


27) Compilation of EU Dioxin Exposure and Health Data  Task 8 – Human toxicology, UK Department of the Environment, Transport and the Regions (DETR)  at


And according to the International Programme on Chemical Safety, based on many studies, "liver damage is a consistent finding among PCB-exposed animals."


28) Section of  International Programme on Chemical Safety, Environmental Health Criteria 140, Polychlorinated Biphenyls and Terphenyls (Second Edition), at


29) WHO | Dioxins and their effects on human health at


30) Public Health England:  Dioxins Toxicological Overview, 2008, Version 1, at

30a) Jones et al., A mortality study of vinyl chloride monomer workers employed in the United Kingdom in 1940-1974, Scand J Work Environ Health 1988;14(3):153-160, in PubMed:


30b) Lagergren et al., Increased risk of hepatocellular carcinoma after cholecystectomy, British Journal of Cancer volume 105, pages 154–156 (28 June 2011), at


30c) American Cancer Society webpage at


30d) American Cancer Society web page at 


30e) web page at


30f) Gounder et al., Cost-effectiveness analysis of hepatocellular carcinoma screening by combinations of ultrasound and alpha-fetoprotein among Alaska Native people, 1983–2012, Int J Circumpolar Health, 2016, at


30g) White and Birnbaum, An Overview of the Effects of Dioxins and Dioxin-like Compounds on Vertebrates, as Documented in Human and Ecological Epidemiology, J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2009 Oct; 27(4): 197–211, at


30h) Carpenter, Ed.: Effects of Persistent and Bioactive Organic Pollutants on Human Health, Wiley, 2013, section on Dioxin-like Chemicals


31) GW Chance, Environmental contaminants and children’s health: Cause for concern, time for action, Paediatr Child Health. 2001 Dec; 6(10): 731–743.(section on Limitations of Risk Assessment) at 


32)  Mayo Clinic Porphyria, at


33)  Balwani and Desnick, The porphyrias: advances in diagnosis and treatment, ASH Education Program, 2012,    at


34) McGraw Hill Medical:  Hematology in Clinical Practice, Chapter 14: Disorders of Porphyrin Metabolism, at 


34a) 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


34b In the Results section, “Serum TCDD concentrations measured at the time of this study in the exposed breast- and formula-fed groups (average, 2.4 ppt and 1.1 ppt, respectively) and their respective comparison groups (average, 1.8 ppt and 1.0 ppt, respectively)


35) At  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.”


36) 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)


37) EPA:  EPA’s Reanalysis of Key Issues Related to Dioxin Toxicity and Response to NAS Comments, Volume 1  (CAS No. 1746-01-6), 2012, p. 4-61 at (Note that 7 x 10-10 mg = .7 pg.)

   In case the above should be difficult for the reader to find or access, EPA public statements from past years on this question have been witnessed and published by the various sources below:

   European Food Safety Authority:  Scientific statement on the health-based guidance values for dioxins and dioxin-like PCBs, May 2015, at

or at 

   Another official record of the EPA's recent RfD for dioxin, from the U.S. Department of Health and Human Services, was found (3/31/2018) in "HHS (U.S. Dept. of Health and Human Services) Comments on 'EPA’s Response to ‘Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment’ Published by the National Research Council of the National Academies,” March, 2010 (PDF) , p. 6, at

   And another record of the EPA RfD of 0.7pgTEQ/kg bw/day is at


37a) Lorber, M. AND L. Phillips. Journal Article: Infant Exposure to Dioxin-Like Compounds in Breast Milk. Environmental Health Perspectives 110:A325-A332, (2002), at


37b) European Food Safety Authority:  Scientific statement on the health-based guidance values for dioxins and dioxin-like PCBs, May 2015, at


38) Patandin et al., Dietary Exposure to Polychlorinated Biphenyls and Dioxins from Infancy until Adulthood: A Comparison between Breast-feeding, Toddler, and Long-term Exposure, Environmental Health Perspectives, Volume 107, Number 1, January 1999, p. 50, at


39) The EPA has fluctuated in its published statements dealing with this RfD for dioxin; there may be pressures from influential people or groups to avoid indicating that a safe level for dioxin is very low; this may be especially due to expected unfavorable comparisons with the much higher exposures that appear to be common. Although the EPA itself may not currently publicize this RfD, it has apparently said nothing in retraction of what it said in the past. And the following sources bear witness to what the EPA said in the past:

-- Patandin et al., Dietary Exposure to Polychlorinated Biphenyls and Dioxins from Infancy until Adulthood: A Comparison between Breast-feeding, Toddler, and Longterm Exposure, Environmental Health Perspectives, Volume 107, Number 1, January 1999, p. 50, at

-- European Commission:  Research & Innovation, Success Stories, Dioxin risk assessment, 26 Feb. 2004, at

-- New Zealand Ministry for the Environment:  Evaluation of the toxicity of

dioxins and dioxin-like PCBs:  A health risk appraisal for the

New Zealand population, p. iv, at

-- National Research Council, Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment (2006), Chapter 5 Cancer, p. 130, The National Academies Press, at

-- EPA:  Review of Draft Documents:  A Cancer Risk-specific Dose Estimate for 2 3 7 8-TCDD and Estimating Exposure to 2 3 7 8-TCDD, p. 2 of second letter, from the Chairman and Co-Chair of the EPA's Ad Hoc Dioxin Panel




40) EPA:  An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000, (Original) EPA/600/P-03/002F November 2006, Table 1-12, at


41) New York Times:  In Rural Areas, the Heat Is on Over Practice of Trash Burning, By Lisa W. Foderaro, MARCH 7, 2005 , at


43)  Lemieux, Evaluation of Emissions from the Open Burning of Household Waste in Barrels, Project Summary, EPA/600/SR-97/134, at


44)  How Regulation and Industry Innovation Have Eliminated Dioxin Emissions from PVC Production and Waste Incineration, by Tobias Johnsen, at

44a) World Bank population density data at  using the data for 1961, which would be closer to the birth years of the cohorts whose data are discussed here.


45) EPA web page, Agriculture: Agriculture and Air Quality: Backyard burning, at


46) When doing a Google search (3/30/2018) for "backyard burning of trash in Europe," the only results in the first 14 pages of listings that dealt with this burning with reference to any region or country were the following:

  -- five articles about this practice in the U.S. (remember, this search was for backyard burning in Europe),


  -- two articles about such burning in India, and


  -- one each regarding this practice in Ireland, Romania, Canada and Australia. 


47) USDA web page "Hispanic Farmers" at


48) U.S. Census Bureau, Overview of Race and Hispanic Origin: 2010, at


49) USDA:  Black Farmers, at


50) U.S. Census Bureau Quick Facts at


50a) USDA:  The Changing Organization of U.S. Farming, 2011, pp. 7-8, at

The percent of farmers who were white women was not specified, but 5% of all farmers were said to be women.


50b) U.S. Census Bureau, A Look at the 1940 Census, p. 9, at


51) Weldon et al., A pilot study of pesticides and PCBs in the breast milk of women residing in urban and agricultural communities of California, Journal of Environmental Monitoring, DOI: 10.1039/c1em10469a, at 


52) U.S. ATSDR, Toxicological Profile for Chlorinated Dibenzo-P-Dioxins, p. 404, at


53)  Shahare:  Techniques for Measurement and Removal of Dioxins and Furans, CRC  Press, Taylor and Francis Group, 2017,. p. 37.


54) Biomonitoring Summary: Dioxin-Like Chemicals: Polychlorinated Dibenzo-p-dioxins, Polychlorinated Dibenzofurans, and Coplanar and Mono-ortho-substituted Polychlorinated Biphenyls  at

55) EPA:  Journal Article: Atmospheric Measurements of CDDs, CDFs, and Coplanar PCBs in Rural and Remote Locations of the U.S. for the Years 1998-2001 from the National Dioxin Air Monitoring Network (Ndamn) , at


55) Backyard burning would be expected to be more likely to take place in areas of low population density than in urban areas for the following reasons:

-- there would be fewer neighbors to be bothered by the smoke in low-density areas,

-- any affected neighbors would be less likely to complain, since they either do it also or else are outnumbered by the backyard burners,

-- local governments are much less likely to prohibit open burning in low-density areas,

-- accidental spread of fire would be of less concern where there are large open areas in which to burn,

-- rubbish pickup services would be more expensive where residences and waste-generating operations (including farms) are far apart.


56) One of the two major types of PCBs is normally called "dioxin-like" because of the similarities of those PCBs' properties and effects as compared with those of dioxins, and dioxins are often grouped together with PCBs when those chemicals are being studied in depth.  EPA: Framework for Application of the Toxicity Equivalence Methodology for Polychlorinated Dioxins, Furans, and Biphenyls in Ecological Risk Assessment,  EPA/100/R-08/004, June 2008 , at


57) Marcus and Krupnik, The Rural Higher-Education Crisis, The Atlantic, Sept. 17, 2017,



58) National Research Council, Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment (2006), Chapter 5 Cancer, pp. 117, 126, The National Academies Press, at


59) CDC: Biomonitoring Summary: Dioxin-Like Chemicals: Polychlorinated Dibenzo-p-dioxins, Polychlorinated Dibenzofurans, and Coplanar and Mono-ortho-substituted Polychlorinated Biphenyls  at


60) Web page at  Even though this source is not peer-reviewed, the 76% figure is highly credible.


61) Finnila, Bone Toxicity of Persistent Organic Pollutants, dissertation presented at University of Oulu, Finland, 2017, at  Especially p. 66.

62) Astur et al., Stress fractures: definition, diagnosis and treatment, Revista Brasiliera de Ortopedia, Volume 51, Issue 1, January–February 2016, at

63) Finnila et al., Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure on bone material properties, Journal of Biomechanics, Apr 2010, at

64) In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects bone tissue in rhesus monkeys, Toxicology, 2008 Nov 20;253(1-3):147-52 at

65) L. Gallagher, High-resolution 'laser x-rays' could spot tiny fractures in bone, Imperial College of London, Aug. 2015, at

66) Jarraya et al., Review Article::Radiographically Occult and Subtle Fractures: A Pictorial Review, Radiology Research and Practice, Volume 2013 (2013), at

67) Riihimäki, Low-back pain, its origin and risk indicators, Scandinavian Journal of Work, Environment & Health, Vol. 17, No. 2 (April 1991), pp. 81-90, at

68) D. Borenstein, Musculoskeletal Signs and Symptoms, Chapter 3  in Primer on the Rheumatic Diseases, JH Klipper Ed.

69) Jamsa et al., Effects of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin on Bone in Two Rat Strains with Different Aryl Hydrocarbon Receptor Structures, Journal of Bone and Mineral Research, 2009, at­­­­

70) Jayson, Difficult diagnoses in back pain, British Medical Journal Volume 288 10 March 1984, at








Appendix A:  Additional evidence related to turns for the worse linked with births during the 1940's, especially in 1949 and later, when PCB and dioxin exposures increased in the U.S.


Remember from Section 1 the exposures to PCBs during the 1940's, increasing after 1945 and especially in 1949 when PCBs were first widely used in building materials.4  This would have affected not only people who lived, worked and went to school in new buildings at that time but also the workers who handled and applied these PCB-containing materials, and their families.  For indications of possible effects of the late-1940's-and-later increases in exposures, see the record of all-cause mortality below:





In all of the above charts, notice the rapidly increasing mortality among U.S. whites born in the years around 1947 to 1950.  

  -- In the first chart, notice the upturn in 2010, when 60-year-olds would have been born in 1950

  -- Among 55-year-olds (middle chart), notice that around 2005, when that age group would have been born in 1950, there was a major upturn in mortality. 

  --  Among 50-year-olds, mortality was declining until what appeared to be an upturn about 1997, implying a turn when that age group would have been born in 1947, at the earlier end of the transitional period. 

  --  Also notice in the Age 50 chart the following:  After a few years of steep increases in mortality among U.S. whites born in 1947 and later, mortality leveled out among those born in 1953 and later.


Notice also in the first two of the above charts (where there were enough years before the upturn to establish a trend) the following:  before the transition to higher all-cause mortality among U.S. whites, there were declines in mortality that seem to have been normal among people born during the 1940's in most countries, but the declines were somewhat less rapid among U.S. whites than among people in almost all of the comparison countries.




Observe in the first two charts above a continuation of the trend seen at the end of the previous charts:  basically level all-cause mortality among U.S. whites. This is seen among people who would have been born in the third quarter of the 20th century, when PCBs were widely used in building materials.  But when seeing data for people born in 1970 and later (in the Age 30 chart), a new, distinctly steeper upward trend in all-cause mortality becomes apparent.  This coincides with U.S. health downturns beginning roughly about 1970, as observed by several authoritative sources.  This gets into a complicated area, which is probably best dealt with in



Appendix B:  Additional information about the early 1940's as a time of significantly increased exposures of developing children to PCBs:


PCBs were first used industrially in 1929.8  There doesn't seem to be a record of how rapidly use of PCBs increased after that.  But considering that the 1930's were the decade of the Great Depression, it is probably safe to assume that use of such a material (even one with many commercial and industrial applications) would not have reached high levels during that first decade of its use.




Darkest areas (on case-deaton final draft map) downstream from GE's PCB pollution are 50 (?)+ miles downstream; (see PCB_HousatonicR file for map) PCBs are first just swept away by current, and LATER become sorbed to particles and are deposited (see USGS article re Housatonic PCB pollution); then they get into groundwater that gets into local wells and/or municipal water supplies?  Also rivers widen downstream and the current becomes slower in the lower elevations closer to the coast, encouraging settling of suspended substances.




As of a 2000 study, the practice of open burning of refuse was not banned or restricted by the majority of the states. << EPA:   An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000, EPA/600/P-03/002F November 2006


U.S. EPA estimates that all-cancer mortality in the United States is increased by anywhere from about 6 per 10,000 to as much as 1.3 per 100 due solely to the current background body burden of dioxin-like compounds. Starr, Significant Shortcomings of the U.S. Environmental Protection Agency's Latest Draft Risk Characterization for Dioxin-Like Compounds, Toxicological Sciences, Volume 64, Issue 1, Nov. 2001, at




"Across demographic categories, the largest increase in opioid overdose death rates was in males between the ages of 25-44." (news release from CDC 4/4/18 at