Comments on Research by Case and Deaton concerning Health Declines and Increases in Mortality among U.S. Whites

 

DP Meulenberg

 

Summary:

Evidence indicates that certain chemicals (dioxins and PCBs), which became widespread in the mid-20th-Century U.S., may have substantially contributed to health declines and early deaths among U.S. whites, such as described by Case and Deaton.  Exposures of developing children to those toxins increased greatly at specific times that are compatible with the beginnings and increases of the midlife health declines that Case and Deaton observed.  Many children could have been exposed to those chemicals during vulnerable stages of their development, in concentrations hundreds of times higher than the levels that the EPA currently considers to be safe.  The children who would have been most exposed to dioxins and PCBs would have fitted (in nationality, ethnicity, and likelihood of graduating from college) the profile of the group that would eventually have high and increasing deaths of despair.

 

Section 1, summary:  Beginnings and increases in adverse health trends, compatible in time with beginnings and increases of exposures to dioxins and PCBs:

 

Case and Deaton observed that mortality among U.S. whites increased greatly among those born after the 1945 cohort; people born in the 1940 cohort and earlier appeared to be unaffected by the increases.  Dioxins and PCBs had become widespread in the U.S. environment during the second half of the 1940's and later, which was in line with the leading role of the U.S. (in the 20th century) in adoption of new technologies.  Therefore many American children who were being born during the 1940's and later were exposed to these toxins during vulnerable stages of their development; many of those exposed children may have become the adults who would later have the increasing health problems and mortality in midlife that were reported by Case and Deaton. 

 

For the complete text on this topic, including references to many supporting peer-reviewed studies and other authoritative sources, go to Section 1.

.

Section 2, summary:  Early childhood is a time of especially great vulnerability to toxic exposures that might lead to pain, despair and/or mortality in midlife.

 

Publications of the U.S. National Academies Press, the EPA, the World Health Organization, the U.S. ATSDR, and a group of 24 experts all point to early life exposures to toxins as having adverse effects in later life.  Such effects, following early exposures to dioxins and PCBs at greatly increasing levels in the mid-20th-century U.S., could underlie the later increases in health problems and early deaths that have been reported by Case and Deaton.  For the complete text, including references to supporting authoritative sources, go to Section  2.

 

 

Section 3, summary:  Effects and potency of dioxins and PCBs:

Dioxins are recognized to lead to liver disease, cancer, suppression of the immune system, and developmental toxicity, all of which could contribute to increases in mortality as well as to pain and other health problems with long-term consequences.  Common infant exposures to dioxins in recent decades have been found to be scores to thousands of times higher than officially-established safe doses.  For full text, including references to authoritative sources, go to Section 3.

 

The ATSDR now ranks PCBs among the top five priority hazardous substances.  The IARC has classified PCBs as carcinogenic, and multiple animal studies have found that PCBs cause liver damage as well as harm to the immune system, reproductive system, nervous system and endocrine system.  Beginning in 1949, PCBs were used in building materials in concentrations up to 8,000 times the current maximum set by the EPA; in addition to emissions by those materials in structures built during the following three decades, exposures could have resulted from workers in construction and other fields bringing these chemicals into their homes on their skin and clothing, exposing their families.  Childhood exposures to PCBs are known to have various effects that could lead to pain in adulthood, which could lead to use (and misuse) of pain-relieving substances, and which could lead to the greatly increased "deaths of despair" in midlife reported by Case and Deaton.  Apparently even miniscule amounts of PCBs and dioxins can have adverse neurological effects on primates, if the exposure is during development, as found in laboratory experiments.

 

For the complete text on this topic, including references to many supporting peer-reviewed studies, see Section 3.

  

Section 4, summary:  Probable locations of especially high exposures to dioxins make a good fit with international differences in the increased health problems reported by Case and Deaton:

 

Case and Deaton found high midlife health problems in the U.S. but much less of those problems in comparison countries, and they found less such problems in large cities than in statistical areas with lower population densities.  Open burning of trash (which typically emits dioxins if plastics are in the mix) is a common practice in rural areas of the U.S. but not in cities, and apparently not in most of the comparison countries; such household burning has been a major contributor to emissions of dioxins in the U.S., mainly since production of plastic products greatly increased in the late 1940's.  Emissions from local household burning are especially hazardous since they are emitted near people and close to ground level.   

 Preview of  Fig. 3

   We should remember the critical windows of vulnerability that occur during early development, as well as the long-term effects of dioxin exposures; then, noticing that this chart (from Case and Deaton 2017) depicts mortality outcomes as of an approximate age of 50, we should consider any environmental toxic exposures that may have been affecting children born roughly 50 years before the time of upturn in mortality for U.S. whites (1997).  After 1945, production of plastics in the U.S. increased dramatically, leading soon to considerable plastics waste to be disposed of, which in turn would have led to much household burning of a kind that is known to release large amounts of dioxins close to people.  Production of plastics in the rest of the world, especially in Europe, lagged far behind that in the U.S., which is compatible with the continued declines in mortality in all of the comparison countries, among people born in those same years. 

Case and Deaton (2017, Table 2) provided a list of 14 countries showing rates of drug, alcohol and suicide mortality increases or decreases in recent years.  There were three countries that were at the second-highest level of increases in this mortality (below only U.S. whites):  Ireland, Canada and Australia.  Those three and the U.S. were apparently the only countries (among the countries being compared) where open burning of trash has been reported to commonly take place, judging by the results of considerable research on the internet.  Looking at those four countries in which backyard burning has been reported to occur significantly, the mortality increases were found to be higher in all of those four than in any of the 10 countries regarding which no reports of common backyard burning were found.  This mortality actually declined in 7 of the 10 countries about which there were no reports of common open burning of trash.

  

 

For complete text on the above topics, including references to many supporting peer-reviewed studies, go to Section 4. 

 

 

Section 5, summary:  Disproportionate exposures to PCBs in the U.S. as opposed to in the comparison countries: 

 

Case and Deaton point to the high level of indications of despair in the U.S., compared with those in six other rich countries that have gone through similar economic stress.  Those differences might at least in part be explainable by adverse effects of PCBs  -- exposures to PCBs were far greater in the U.S. than in the other countries, as indicated by good evidence.  For complete text on the above topic, see Section 5.

 

Reference is made to two appendices that deal with other matters discussed by Case and Deaton: 

Appendix H:  Disproportionate effects of the toxins on whites compared with African-Americans and Hispanics 

 

Appendix I:  Disproportionate effects of these toxins on children of non-degree-pursuing families

 

 

 

Section 6, summary:  Dioxin exposures as related to urban-versus-rural differences, in parallel with health declines:

Case and Deaton found that all-cause mortality increased substantially in the four least-densely-populated of six residential classifications, whereas mortality declined in the largest metropolitan category.  There is good reason to consider the possible existence of a benefit of residing in large areas with high population density, as compared to in areas with substantial percentages of rural population.

  Preview of Fig. 10

   

This is a modified version of a map in which Case and Deaton showed increased mortality (indicated by darker areas) in various parts of the U.S.  (The modifications are the blue markings and place names, which were not in the map as provided by Case and Deaton.)  There are clearly north-south differences, which will be discussed in the next section.  In a large majority of the cases of the local areas that are lighter in color (meaning lower mortality), those locations have higher population density; that is indicated by the many city names identifying the locations where mortality is lower, as well as by U.S. Census Bureau data. 

Lower mortality in areas of higher population density very likely has much of its origins in the following:  Domestic burning of trash, which is known to the EPA to emit considerable dioxins close to people, is widely practiced in U.S. rural areas but not in densely-populated areas.  And many developing infants are thereby exposed to dioxins in concentrations exceeding established safe levels by scores to thousands of times. 

For complete text on the above topics, go to Section 6.

Section 6.a, preview:  Apparent exceptions to the link between mortality and population density, where statistical areas are too large to show local variations in mortality.  For complete text, see Section 6.a.

 

Section  6.b, preview:  Where mortality data is shown in at least moderate detail, and where industrial and other potent sources of dioxins are not major factors, the link between population density and mortality is even more consistent:

Preview of  Fig. 11

The above is just one demonstration of the mortality/ population-density connection, numerous examples of which can be found with close examination of the appropriate maps.  For full text on this topic, see Section 6.b.

 

Section 6.c, summary:  Exceptions to the link between low population density and high mortality, and how those exceptions appear to support a causal relationship between dioxin emissions and increased mortality.

-- Some exceptions appear to be related to state laws and local ordinances that restrict backyard burning, thereby reducing dioxin emissions in low-population-density areas,

-- Some exceptions are apparently related to other EPA-recognized major sources of dioxin emissions, such as iron and steel industry; these sources might create dioxin emissions in high-population-density areas at levels similar to what would result from trash burning in rural areas.

-- Some exceptions could result from climate differences that affect amounts of airborne dioxins and PCBs.

  

Overall, it appears that comparative dioxin exposures may be the predominant factor underlying geographic differences in mortality.  Low population density is very likely linked with mortality only because it is the primary determinant of where private burning of trash takes place widely, emitting considerable dioxins next to ground level and close to people.

 

 

For complete text on the above topics, including references to many supporting peer-reviewed studies, see Section 6.c

 

Section 6.d, summary:  Household trash burning other than in backyards could lead to even worse dioxin exposures:

 

Backyard barrel burning was found in a survey to be lower in northern Minnesota than in the southern part of the state, yet mortality was found to be higher in the northern section; so this at first seems to be in contradiction with the normal link between dioxin emissions and mortality.  But the survey also found that trash burning indoors or next to houses was far higher in the northern part of the state than in the south.  So this turned out to be fully compatible with the link between dioxin emissions and mortality.

 

For complete text on this topic, with references to supporting documents, see Section 6.d

  

 

Section 7, summary:  Harmful exposures related to climate  differences:

 

There appears to be some general similarity between the geographic pattern of increasing mortality (as found by Case and Deaton) and the pattern of climate zones in the U.S.

Figures 7 and 8 side-by-side

 

 

It is probably relevant that exposures to dioxins on average are greater in warmer areas, since those chemicals are better removed from the air (by deposition) where temperatures are colder.  Also, PCBs, which are chemically related to dioxins, are known to be volatilized far more where temperatures are higher.  Airborne dioxins can be very important contributors to body levels of those toxins, as indicated by the finding that workers in some chemical plants were found to have dioxin levels hundreds of times higher than average.

 

For complete text on the above topic, including references to supporting peer-reviewed studies, see Section 7.

 

Section 8, preview:  Mortality was found to be increasing faster in white non-Hispanic women than in white non-Hispanic men, according to Case and Deaton.  This, too, is explainable on the basis of dioxin exposures, which have been found in studies to affect females much more than males, in various ways.  For complete text on this topic, including references to supporting peer-reviewed studies, see Section 8.

 

Section 9, preview:  Other health declines, including sciatica:  Adverse health effects of dioxins have been found to include bone toxicity, particularly during development.  That, combined with effects of PCBs in damaging cartilage, could help explain the increases in sciatica among those with less than a BA, as have been reported by Case and Deaton.  For complete text on this topic, including references to supporting peer-reviewed studies, see Section 9.

 

Section 10, preview:  Other types of pain resulting from combined effects of dioxins and PCBs:

For complete text on this topic, including references to supporting peer-reviewed studies, see Section 10.

 

 

Conclusion, preview:

This article has suggested that the following deserve close attention as possible causes of the reported health declines and mortality increases:

 

   a) the (past) widespread intentional use of PCBs, which resulted in substantial close personal exposures, with exposures still continuing due to PCBs' persistence in the environment, and

 

   b) local burning of plastics-containing trash, emitting dangerous concentrations of dioxins, mainly in low-population-density areas; this practice continues in the rural U.S.

 

.  The mid-20th-century explosive increase in use of disposable plastics in the U.S. led to hazardous emissions of dioxins via household and farm burning, which in turn led to intakes of dioxins by infants at high levels during vulnerable stages of development.

 

   Exposures of developing children to PCBs, resulting from former widespread uses in concentrations hundreds to thousands of times the levels that are currently considered safe by the EPA, also increased greatly beginning in the late 1940's. 

 

   Both dioxins and PCBs are known to have effects that may have led to the increasing mid-life health problems and mortality observed in later decades.  

 

   Exposures to both dioxins and PCBs would have been much greater in the U.S. than in the comparison countries, which parallels the differences in health and mortality data observed by Case and Deaton.  Similarly, exposures to both of those toxins would have been much greater for white, working-class families than for minorities or for children of college-degree-pursuing families. 

 

A lesson might be learned about the responsibilities of technological leadership, based on what transpired following wide distribution and use of plastics and PCBs in the mid-20th century U.S.:  When preparing to introduce new products that might conceivably end up releasing chemicals with which we don't already have extensive experience, caution should be exercised to anticipate all potentially adverse outcomes; thorough testing should be carried out on all substances that might be anticipated to end up in the environment as a result of distribution of the new materials.

 

For the complete conclusion, with links to supporting sections in the body of the text, go to conclusion.

 

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 Comments on Research by Case and Deaton concerning Health Declines and Increases in Mortality among U.S. Whites

(Complete Text)

Introduction:

Evidence indicates that certain chemicals (dioxins and PCBs), 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 scores to 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 dioxins and 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.

 

Section 1:  Beginnings and increases in adverse trends, compatible in time with beginnings and increases of exposures to specific toxins:

Fig. 1

 

.

Notice in this graph (from a 2017 document by Case and Deaton^1d) that, following insignificant changes in drug, alcohol and suicide mortality in 1935-1940, there were

    (a) a very minor increase with the 1945 cohort and

    (b) major mortality increases among those born in the next cohort (1950) and later.

Fig.2

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 in the late 1940's and later.  The point on the red line for the year 2000 should be focused on, as an approximate time when minor increases in mortality started to become greater increases.  The 50-54-year-olds whose mortality data is shown at the point for the year 2000 would have been born in 1946 to 1950.  Mortality of those born after 1946-1950 would show up in the rapidly-rising section of the red line.

 

So there apparently was a major transition in which lives of many children born and developing in the U.S. during the 1940's, especially those born in the late 1940's and later, would end up worse than those of similar people born in earlier years.  

 

For additional data indicating that this was a period of transition that is relevant to current 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 outcomes in adulthood.¹  (That will be discussed more in Section 2.)  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 decade of the 1940's and that (b) became more prominent in the environment in the late 1940's and later.

 

Dioxins and PCBs (polychlorinated biphenyls) both fit that description. 

Dioxins are recognized to have various harmful effects including damage to the liver (see Section 3), which could be a source of the above-discussed mortality increases and desire to escape pain; these toxins became significant in the environment after 1940, according to the U.S. ATSDR (Agency for Toxic Substances and Disease Registry).²¹  Exposures to dioxins would have increased especially after 1945, because (a) burning of vinyl chloride plastics is known to the EPA to emit dioxins;²⁶ (b) production of plastics in the U.S. (especially in consumer goods) expanded "explosively" after the end of World War II (1945), according to a history of plastics in Scientific American;²² and (c) within a couple of years after that, there almost certainly would have been considerable trash consisting of disposable vinyl chloride plastic products, including toys and packaging,²³ to be disposed of; much of that would have been burned in municipal waste incinerators, hospital waste incinerators, and in backyard burning, all of which are known to the EPA to emit large amounts of dioxins.^23a  During the 1950's, many more companies started to produce PVC plastics, and volumes increased greatly during that decade.²⁵  Efforts to reduce dioxin emissions from municipal and hospital waste incineration in the very late 1900's were rather successful; but backyard burning, which is common only in rural areas, has continued to be widespread and a very major source of dioxin emissions.^23a  

 

 

PCBs:  The ATSDR now ranks PCBs among the top five priority hazardous substances.^1c (For recognized health effects of PCBs, including leading to pain, see later.)  Production of PCBs (not yet known to be toxic at that time) began in the 1920's but only reached substantial volume after 1945, according to a working group of the International Agency for Research in Cancer;^1e  they were used in various kinds of equipment and in many areas of manual work.⁷   Of the nine countries (including the U.S.) that started production of PCBs before 1960, total production in the U.S. equaled the total for all of the other eight countries combined.^1e  Exposures became still greater in 1949 and later, when PCBs came to be used in various types of building materials.⁴  

 

The developments described above are part of a larger picture:  The U.S. has become first in widespread adoption of new technologies;^22b accordingly, Americans have led in experiencing unanticipated health effects of the new technologies.  Technological advances in the early 20th century led to (a) products that were made of plastics and (b) products in which PCBs were intentionally included, because of the useful properties of that chemical.  Both of these product types quickly became so widely distributed in the U.S. after 1945 that much of the American population was exposed to the (then unknown) toxic effects of chemicals that were either contained in the products or potential results of the products' eventual disposal.  Developing children, who are especially-sensitive to long-term effects of chemicals such as dioxins and PCBs, were among those exposed, including via their parents.  The considerable adverse health effects of both types of toxins were only discovered decades after the rapid increases of the exposures had started.  

 

 

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).  The EPA also discusses developmental toxicity as being distinctly a characteristic of dioxins, saying that this is supported by many different kinds of scientific observations.^21a

 

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  The U.S. ATSDR states that "there are critical periods of structural and functional development during both pre-natal and post-natal life, and a particular structure or function will be most sensitive to disruption during its critical period(s). Damage may not be evident until a later stage of development."^2b  A group of 24 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 

 

Latency would be an especially significant characteristic of immunotoxicity, the recognized effect of PCBs mentioned just above; the results of reduced immunity could go relatively unnoticed during the relatively sheltered years of childhood but could have serious effects following occupational, traffic-related, and other exposures to toxins over the extended course of adult life. 

 

Other effects of childhood exposures to PCBs that may lead to despair in later life are discussed in Appendix C.

 

In a discussion of vulnerability of the early developmental period to toxins, which can lead to disease and pain in adult life, latency of effect is an obviously important sub-topic.  There is much on that subject as related to dioxins, and rather than devoting space to that here, that will be discussed in Appendix E.

 

 

Section 3:  Effects and potency of dioxins and PCBs, related to findings of Case and Deaton:

 

Dioxins:  Case and Deaton (2015) found increases in chronic liver disease, as well as increases in all-cause mortality, among most age groups of the adult population but not among older people.^17b  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 on their list being liver damage, followed by suppression of the immune system and cancer.  Also high on their list is developmental toxicity, followed by the explanation that "newborn offspring of several species have been shown to be particularly sensitive."²⁷   According to Public Health England, reported effects of dioxins also include 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  The International Agency for Research on Cancer (IARC)²⁹ and the National Toxicology Program have classified dioxin as a known human carcinogen.  In 1991, the U.S. National Institute of Occupational Health and Safety, in its cancer mortality study of US workers exposed to dioxin, reported that mortality was increased from all cancers combined among those workers, particularly among those with the longest occupational exposure to dioxins and those with the greatest latency from exposure.^30g 

 

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 mothers' bodies.  Studies of infant exposures to dioxins in many other countries have found data in the same order of magnitude; almost all of the studies finding infants to be commonly exposed to high levels of dioxins were carried out in 2000 and later, decades after environmental emissions of dioxins were reported to be declining.^38a  A 2013 document of the UN Environmental Programme states that exceedances of established safe levels of dioxin exposures by breastfeeding are in the same range as indicated above.^38f

 

The ATSDR notes 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." (ref. 2b, p. 345)  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 exposures to dioxins at levels that are only moderately above average in current times.  Also remember from Section 2 that early childhood is a period of especially great vulnerability to long-term effects of toxins.

 

PCBs:  Remember that the ATSDR now ranks PCBs among the top five priority hazardous substances.^1c   The IARC has classified PCBs as carcinogenic, and multiple animal studies have found that PCBs cause liver damage;^38b also, PCBs have been found to affect an animal’s immune system, nervous system and endocrine system.^38c  Human studies also, according to the CDC, have found PCB exposure to be associated with various cancers, especially liver cancer.^38c  In relation to the greatly increased "deaths of despair" in midlife reported by Case and Deaton, childhood exposures to PCBs are known to have various effects that could lead to pain or distress in adulthood, including harm to the blood brain barrier and to cartilage (thereby leading to joint pain) and reduction of activity levels (activity is authoritatively recommended to reduce pain).  (Details and references in Appendix C.)  

 

Of the scores of former intentional uses of PCBs, their use in building materials (beginning in 1949)⁴ would have led to especially high exposures.  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.  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 (up to 10,000 times) greater than levels typical of ambient air (citing five studies as evidence);^1f and other evidence indicates major increases in blood levels of PCBs resulting from this exposure.^4a  Construction workers and people in other fields working with PCBs would have brought these chemicals into their homes on their skin and clothing, exposing their families.^1b  

 

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 1/100,000^th 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 so 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.  

 

PCBs have been found to be present in human milk in doses 63 to 270 times the minimal risk level established by the U.S. Agency for Toxic Substances and Disease Registry.^38d

 

The above 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 4:  Probable locations of especially high exposures to dioxins make a good fit with national differences in 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.  As will be discussed in more detail below, open burning  of trash is a common practice in the rural U.S. but apparently not in most of the comparison countries and not in cities; and that practice has been of major significance in emitting dioxins that may have been substantial causes of the health declines described by Case and Deaton.  (See below)

 

Open burning of plastics-containing trash in rural areas would have begun on a large scale after plastics came into the waste stream during the 1940's,²¹ especially after 1945 in the U.S.,²² and later in Europe.²³  That would have resulted in exposures of children to dioxins^23c beginning in the late 1940's while children born in that period were going through their vulnerable developmental periods.

 

The EPA reports that burning of trash is a major source of dioxin emissions;^40,40a the NIH points out that numerous household, medical and construction products and materials contain PVC plastic, which emits dioxins when burned;^40c trash since the late 1940's would typically have contained plastics as well as coated paper.  Backyard burning in barrels, which is probably difficult to distinguish from other household burning (trash burning is often done without a barrel^40b), is common in rural and non-urban U.S., according to the EPA and the New York Times;^40a,41 also common is the practice on U.S. farms of burning the large plastic wraps that cover hay bales.⁴¹  The EPA considers backyard barrel burning to be the largest quantifiable source of dioxin emissions in the U.S. as of the latest national inventory.^23a  Compared with combustion in municipal incinerators, open burning typically takes place mainly in the lower end of the temperature range, where dioxins are most readily formed.  As indicated in a study published by the EPA, 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.⁴³   

 

But the problem with emissions from household and farm burning is only partly due to the quantity.  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 emissions from household burning, at cooler temperatures and emitted close to the ground; and (as stated in the above-cited study) there is "concentration of these emissions in the local neighborhoods due to poor dispersions."⁴³  Concentration of the dioxin emissions in local neighborhoods would apply especially in valleys, where rural towns are often located.  An 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

 

An urban-rural divide in the practice of backyard burning is as would be expected for various reasons, such as

  -- comparative numbers of nearby neighbors who could be adversely affected by smoke and fire hazard from a neighbor's burning,^55a and

  -- municipal ordinances forbidding outdoor burning of trash.

 

When considering possible effects of dioxin exposures, we should keep in mind the special vulnerability of developing children (see Section 2) as well as the evidence about specific harmful effects of dioxins as presented in Section 3; it is also relevant to review the dioxin doses that have been determined to be relatively safe, as compared with actual exposures received by developing children:  actual exposures of developing children have very often exceeded established safe doses by scores to thousands of times. (This topic was covered in Section 3.)  

  

Time of the upturn in mortality in the U.S., and how that could be related to backyard burning:

   Fig. 3

In this chart from Case and Deaton (2017),^1d we can see mortality data for people of approximate age 50 at different points in time.

 

Mortality outcomes clearly differ significantly according to when people in that group were born.   To determine the approximate birth years of the people whose mortality data is shown at specific places on a line, just subtract 50 years (the average age) from the relevant year shown on the horizontal axis.  It is easy to see the unfavorable upturn that took place in all-cause mortality among U.S. whites born after about 1947, in contrast with the continued declines in mortality in all of the comparison countries. 

 

Remember (from Section 2) about critical windows of vulnerability occurring during early development; and bear in mind (from Section 3) the long-term effects of dioxin exposures, including liver damage, reduced immunity, and cancer.  With the above in mind, it should then be of interest to review what was taking place 50 years before the adverse turn shown in this chart:

 

Production of plastics increased dramatically in the U.S. after 1945, according to a history of plastics in Scientific American.²²  (Production of plastics increased much more slowly in the rest of the world, especially in Europe where it did not increase significantly until after 1960, and even after 1960 plastics production in Europe increased very slowly.^22a)  The increase in U.S. plastics production would have led to considerable waste to be disposed of; this in turn would have led to much open burning of plastics-containing trash (in rural U.S.) of a kind that is now known to release large amounts of dioxins in close proximity to people.  Allowing for the expected lag after initial major production of these plastics before large amounts would end up in backyard burning, after 1947 is about when one would expect to see the start of a major increase in early developmental exposures of U.S. children to dioxins resulting from open burning of the newly-widespread disposable plastics.  Such exposures in other countries, especially in Europe, would have lagged far behind those in the U.S. (see above) if they were to occur at all, depending on practices of open burning of waste.

 

Remember also (from Section 1) that production of PCBs, also, first reached substantial volume after 1945.^1e 

 

With the above in mind, it should be of interest to find out about the health outcomes, later in life, of those who were born in 1947 and later.  In Figure 3 (above left) we can see depiction of mortality outcomes of U.S. whites born before and after 1947, when those people are at an approximate age of 50; the left section of the red line shows mortality data for those born before 1947 on average, and that shows declining mortality in midlife; the right-hand section of that line shows mortality outcomes for those born after 1947 on average, and that shows increasing mortality when those people are in midlife.  That difference in health outcomes, according to before-versus-after-1947 birth-year, is exactly as would have been predicted on the basis of

   a) knowledge that plastics in trash would have been newly substantial in the U.S. in the late 1940's (see above),

   b).awareness that dioxins are emitted by burning of plastics (see Section 4), and

   c) knowledge of harm caused by developmental exposures to dioxins (see Section 3).

  

What was happening in comparison countries in this area:  It is revealing to look at the data for the 13 countries used for comparison in Case and Deaton (2017),^1d Table 2.  There were three countries that were next highest (behind only U.S. whites) in the drugs, alcohol and suicide category of mortality increases:  Ireland, Canada and Australia.  In that regard note what was found from 13 different substantial online searches for articles about backyard burning of trash (including many searches carried out using the dominant country-specific search engines):  those same three countries were the only ones among the 13 comparison countries where this kind of burning was reported to commonly take place. (For details of the searches, see Appendix K)

 

In the category of mortality increases discussed here, outcomes were worse in all of the four countries in which backyard burning is reportedly common (including the U.S.) than in any of the 10 countries regarding which there is no online mention of common backyard burning. (see Table 2, Column 2 at ^1d) 

 

It is conceivable, although unlikely, that the above was merely a chance occurrence.  But there appears to be no question that this type of burning produces dioxins in amounts that are hazardous to nearby people. (see earlier)   And plastics, emitting dioxins when burned, would have been increasingly present in the waste stream during the vulnerable developmental periods of the people whose mortality trends were being reported in midlife. (see earlier)

 

As reinforcement for an inference that the U.S., Canada, and Australia are all countries in which household burning of trash would be common, while that practice is uncommon in 10 comparison countries, consider the following:  The founding immigrants to America, Canada, and Australia were largely people who departed from their home countries and journeyed very long distances, often to unsettled, hazardous areas.  That probably typically involved considerable risk and hardship in order to pursue an uncertain future; and people who decided to do that were likely to have been motivated at least in part by a strong reluctance to conform to what was customary in their home countries, in religious belief or other areas.  They would very likely have had  relatively little concern about personal comfort but great respect for the value of personal freedom to do as one chooses; those traits very likely carried on as part of the new cultures created by the settlers.  On the other hand, an inclination to conform to preferences of surrounding people was more likely to prevail in the cultures of those who stayed behind. 

 

One can then consider which countries' populations would be likely later to consist to a great extent of people who feel strongly that it is their right to act as they see fit on their own property.  For many citizens of the U.S., Canada, and Australia, if there is no certainty of a result worse than temporary discomfort to others, while there are clear financial benefits of burning versus alternative disposal methods,⁴¹ it could be difficult to convince them not to burn.

 

...............................................

 

The above has focused on the probable role of dioxin exposures in contributing to mortality increases in the U.S.; but effects of dioxins would be difficult to separate from effects of  the similarly-toxic PCBs, exposures to which were also increasing very disproportionately in the U.S. in the late 1940's.  Remember that production and use of PCBs first reached substantial volume after 1945 and occurred mainly in the U.S.;^1e as was the case with dioxins, this increase of exposure coincided with the birth years of U.S. whites who would later (in midlife) have increasing all-cause mortality.

  

 

 

Section 5:  Disproportionate exposures to PCBs in the U.S. as opposed to in the comparison countries, in three respects: 

.

Case and Deaton point to the high level of indications of despair among U.S. whites, compared with the lack of such indications in six other rich countries that have gone through similar economic stress. (Remember from Figure 2 about that.)

 

The national differences might at least in part be explainable by health effects of PCBs -- remember that the ATSDR considers PCBs to be among the top five priority hazardous substances,^1c and bear in mind that pain is likely to be a long-term result of PCB exposure (see earlier, in Section 3).  Exposures to PCBs were much greater in the U.S. than in the other countries, as indicated by the following:

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

Fig. 4

 

(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 mostly-red color of the U.S., as compared with the lack of red in Canada and most of Europe; all four of the European countries with comparatively favorable mortality trends are located to the north of red areas.

 

When looking at this map one should remember that, for decades during the sensitive developmental periods of today's mid-life people (Section 2), building materials were used that exceeded the current EPA maximum for PCBs by thousands of times (see PCBs in Section 3); that is the context in which one should think about the PCB emission rate's increasing 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 used; there was at least one PCB application that was unusually widespread in the U.S. compared with usages in most of the comparison countries --  that of asphalt roofing materials.^8a  A substantial amount of PCB-containing material directly above the heads of millions of people, and directly exposed to heat from the sun, 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 roofing 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. 5

 

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. 6

 

 

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. (The case of Australia is discussed further in Appendix D.)

 

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 shingle roofing that was widely applied in the U.S. in earlier decades; and all of those countries had much lower 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 (in line with the relationship we are seeing) the UK and Canada both had substantial unfavorable trends in the mortality that Case and Deaton studied (^1d p.15, and a close look at Figure 2 earlier would show that also).  The U.S., also with mostly asphalt roofing, had a trend in that mortality that was even more unfavorable than the trends 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).

 

For a more extended discussion of the relationship between PCB exposures and mortality results among the countries discussed, see Appendix B.

.......................................

 

Case and Deaton found disproportionate health declines among non-Hispanic whites compared with African-Americans and Hispanics.  Dioxin exposures from the common rural practice of open burning would have affected mainly farmers, who are very disproportionately white; and PCBs were extensively used in manual trades that were disproportionately white.  To read more on this topic, with references to peer-reviewed and other authoritative evidence, see Appendix H. 

 

Case and Deaton also found disproportionate health declines among people with less education as compared with people with bachelors' degrees.  PCBs were formerly intentional components of materials extensively used in manual trades, and dioxins from rural burning of waste would have affected mainly farmers; people employed in both of the above occupational categories are usually not college graduates.  To read more about the above, with references to peer-reviewed and other good evidence, see Appendix I.

 

 

 

Section 6:  Dioxin 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 in Section 2); then notice the findings of Case and Deaton (2017^1d p. 21) indicating that   

  --  mortality increased on average one per cent per year in the four least-urban of six residential classifications (those with the lowest population densities),

  --  mortality did not increase in the category with the second-from-highest population density, and                                                                                          

  --  mortality actually fell in the category with the highest population density.

 

(This will be discussed more later.)

 

The above should bring up the question as to whether there could be some benefit, related to this recent mortality trend, in residing in large areas with high population density.  It turns out that there is considerable reason to suggest the existence of such a benefit, with good evidence explaining why it should be that way.

  

Figure 1.9 from Case and Deaton (2017),^1d shown below, depicts the most recent all-cause mortality data for white non-Hispanics ages 45-54, showing areas with higher mortality rates as darker areas..

Fig. 7

 

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. 8

 

 

 

Possible reasons for a causal relationship between mortality differences and climate zones will be discussed later, in Section 7.

 

Bypassing for now the wide-scale effects of climate, we will go into some details in the mortality data that merit closer looks in a search for possible causes of mortality increases.  A close examination of the Case and Deaton map in Figure 7 above, combined with knowledge of regional variations in population density (see below), shows that local areas of lower mortality are normally areas of high population density (mainly cities or groupings of cities).  So a look at a map from the U.S. Census Bureau depicting population density might be helpful.

 Fig. 9

  
 

 

The above map shows high population density conspicuously in two large areas where, as shown earlier in Figure 7, mortality is unusually low:  the Southwest coastal area and the I-95 corridor in the Northeast.  In addition, the great majority of all areas shown with high population density (above) also have relatively low mortality (see below, marked with blue).  (These higher-density/lower-mortality areas are also indicated below by names of cities at those same locations.) 

.  

Fig. 10

 

So there appears to be strong link:  In areas of greater population density, mortality is normally lower.

 

 

Section 6.a:  Apparent exceptions to the above correlation, where statistical areas are too large to show relevant local variations in mortality.

 

Some apparent exceptions to the above generalization occur in places in which the statistical areas showing the mortality variations are too large to show local differences.  Examples above are in the Northwest (Boise, Idaho and  Billings, Montana) and also in New England; individual statistical areas that incorporate most of Massachusetts (in one) and half of New Hampshire (in another) prevent data from individual cities in those regions from showing up.

But a different, more detailed map showing mortality data within the relevant period, such as the one for the year 2000 on the left (also from Case and Deaton 2017), might allow the normal higher-density/lower-mortality relationship to be more observable.  (See Boise and Billings showing up lighter than surrounding areas in this map.)  So at least some of what might appear to be exceptions to the higher density/ lower mortality correlation turn out, with more precise data, not to be exceptions at all.  That very likely also applies to other apparent exceptions, especially where the statistical areas are very large, which is the case especially in much of the West.

 

Section 6.b:  Where mortality data is shown in more detail, and where industrial and other sources of dioxins are not substantial, the link between population density and mortality is more apparent:

 

 Fig. 11

 

  

The above is merely one of dozens of examples of the association between population density and mortality that can be easily found with close examination of the Case and Deaton mortality map (Figure 7) combined with the Census Bureau population density map (Figure 9) and/or U.S. cities maps.

 

What is discussed above might be discounted on the grounds that it is merely visual evidence, based on what appear to be local variations.  But essentially the same mortality/density relationship was found in strictly numerical, nationally-summarized data from Case and Deaton, in reporting about comparative mortality rates among six different residential classifications (p. 21 of ref. 1d). (For details, see Appendix G.)   The results were compatible with what would be expected if there had been a major source of exposures to developmental toxins in low-population-density areas, such as backyard burning after it came to include plastics (see earlier); this was a source that was new in the mid-20th century when people were being born who would later have increasing health problems and midlife mortality. 

 

On the other hand, there are obviously cases in which mortality is not accurately predicted by population density.  Before considering those, we should first try to better understand why mortality usually seems to be higher where population density is lower; remember from earlier that developmental exposures to dioxins are known to often have serious long-term health effects (see Sections 2 and 3), and dioxins are known to be emitted in especially hazardous concentrations close to people in rural locations, via burning of trash that contains plastics. (see earlier, in Section 4)

 

And we should bear in mind that such developmental exposures to dioxins in U.S. rural areas would have greatly increased at a time (after 1945 -- see earlier) that is fully compatible with the major increases in mid-life mortality that were to occur eventually among those born in the late 1940's and later (see Figure 3 and accompanying text).

 

To sum up:  Rural location serves as an approximate indication of harmful dioxin emissions by way of trash burning, a practice that is common in rural areas.  Higher population density normally means less trash burning, which usually means less dioxin emissions close to people; and a result of that appears to be lower mortality. 

 

However, as will be discussed next in Section 6.c, there are local areas where other sources of harmful toxins may be as serious as trash burning; and there are substantial variations in methods and locations of trash-burning, which could lead to major local differences in harmful emissions resulting from that same basic practice.  So there are significant imperfections in the ability of population density to predict mortality differences, but it appears that differences in dioxin exposures are generally accurate in predicting differences in mortality, as will be discussed in the next subsection.  We will now look at individual locations to see whether expected dioxin exposures from sources other than backyard burning could predict mortality differences in those locations.

  

Section 6.c:  Exceptions to the connection between low population density and high mortality, and how those exceptions may support a causal relationship between dioxin emissions and increased mortality.

 

Bear in mind that the proposed reason why low population density correlates well with higher mortality is because of high dioxin emissions from household trash burning in rural areas, in close proximity to people.  But there are also many other sources of dioxin emissions which, if sufficiently concentrated, might have effects equal to or greater than the effects of the backyard burning.

 

 --  In Figure 9, the population-density map, the (formerly) heavily iron-and-steel production areas including Gary, Indiana and Cleveland/Youngstown/Canton, Ohio, and Pittsburgh, Pennsylvania all show up as having high population density; but none of them show low mortality, as most other high-population-density areas do.  Iron and steel is one of the principal industries known to the EPA to emit dioxins in substantial amounts;^24j it appears that pollution levels in those cities may have been sufficient, when people who died prematurely in the early 2000's were being born, to cancel out the benefit to developing children of not having backyard burning taking place where they lived.

 

  --  Other low-mortality areas show up in Figure 10 even in low-population-density areas in Vermont, Wisconsin and Minnesota; in that regard, it should be noted that open burning of trash is prohibited in the entire state of Vermont^24b and open burning of most trash is prohibited in Wisconsin^24g and Minnesota.^24h  But there are limitations to the usefulness of this kind of information:  prohibitions of open burning are also in place in some other states, and existence of individual state prohibitions is not necessarily meaningful since (a) they may have been enacted too recently to have an effect on currently-published health data, (b) they sometimes contain significant exemptions, and (c) they are complied with only moderately, at least as found by a survey in Minnesota.^24m  So, in the absence of detailed information, discussion of effects of governmental prohibitions is meaningful mainly in limited cases, such as when information from several states is combined, as was the case just above.  

 

Governmental restrictions may also be useful in understanding outstanding differences in mortality, as in the case below.

Fig. 12

 --  A sole low-mortality location can be seen in the very non-urban middle of Pennsylvania,  as shown in Figure 12 on the left.  That is Centre County, which includes the borough of State College, the largest town in that county. 

 

This is an exception to the usual linkage of low-mortality (Figure 7) with dense population (Figures  9 and 10).  But research into this matter reveals that open burning of waste is generally prohibited in Centre County, whereas it is permitted by and widely practiced in the state of Pennsylvania.  (Details in Appendix F)   Low mortality is not linked with high population density in this case, but it is linked with the causal factor that apparently underlies the effect of population density on mortality:  household burning of plastics-containing trash is prohibited, which in this case apparently successfully prevents the burning that would typically otherwise be emitting dioxins close to people in non-urban areas. (See Section 3) 

   

  

So it appears that, where mortality is not accurately predicted by population density, it can more accurately be predicted by the likely underlying cause of the mortality differences -- variations in dioxin emissions:

  --  below-normal dioxin-emitting burning of trash, as in the cases of Centre County and Vermont, Minnesota and Wisconsin, or

  --  unusually high other sources of dioxins, as in the cases of the (former) major iron and steel-producing cities.  Another example of this is discussed below.

 

 

Section 6.d:  Household trash burning other than in backyards could lead to even worse dioxin exposures:

 

Burning of trash indoors or next to a house is probably an even more serious source of health problems than burning in backyards, and one that the EPA does not seem to have dealt with.  This can be seen with reference to indoor burning practices in Minnesota, observing how such practices relate to mortality outcomes.  (See just below.)

   Fig. 13

Areas of higher and  lower mortality for the state of Minnesota are shown by darker and lighter shadings in this enlarged segment from Figure 7.  Clearly, the southern parts of the state have significantly lower mortality than the northern half.  So it may be surprising at first to see (according to a survey, in Figure 14 below) that in the northern sections of the state (NW and NE) there is less barrel burning of waste than in the southern sections. 

Fig. 14

But it turns out that higher mortality in northern sections should have been expected, since burning of waste in stoves and fireplaces is several times higher in the northern sections of the state than in the southern sections.  As bad as emitting dioxins in one's backyard is, it would be even worse to emit them (a) indoors, from a fireplace or indoor wood-burning stove, or (b) by means of a device (an outdoor wood boiler/stove) that is intended to burn at relatively low temperatures and which would therefore be expected to emit more dioxins; such stoves also emit from a low stack, normally close to a house.²⁴ⁿ

 

Bear in mind that the strong association between lower population density and higher mortality (see Figures 9 and 10) is very likely caused by trash-burning practices that are common in rural areas.  In the one case in which a survey has been published concerning waste-burning practices in detail (just above), the correlation between dioxin-emitting burning practices and mortality outcomes appears to be affirmed by close examination of the data.  The most hazardous trash-burning practices (the ones that emitted the most dioxins closest to people) correctly predicted mortality differences. 

 

Notice that the association between mortality and the most hazardous trash-burning practices in the above case was not merely an overall north-south regional relationship; it also held true with respect to each of the four corners of the state independently.

.   

 We should remember the following from earlier: 

   --  There are good reasons to believe that dioxins from trash burning would be able to cause later mortality increases:  As explained earlier (Section 2), infancy is well recognized to be a stage of development that is especially vulnerable, when long-term health can be endangered by toxic exposures.  And common exposures to dioxins distinctly during infancy have been authoritatively determined to be high enough to exceed established safe levels by scores to thousands of times. (Section 3). 

 

  --  The time of the major increase in rural household burning of plastics (see earlier), including dioxin emissions at hazardous levels, makes a perfect fit with the time of transition from declining mortality to rapidly increasing mortality.  As reported by Case and Deaton (2017, pp. 17-18, ref. 1d), 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.

 

 

 

Section 7:  Harmful exposures related to climate  differences:

 

Remember from Figures 7 and 8 earlier (shown again below, reduced) that there appears to be a general similarity between the geographic pattern of mortality (as found by Case and Deaton) and the pattern of climate zones in the U.S.

Review of Figures 7 and 8

 

 

Although the relationship of climate zones to mortality is only approximate, it should give us something to think about.  One likely source of a climate-mortality relationship has to do with exposures to dioxins and PCBs 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 be 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 mentioned 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  Remember from Section 1 that PCBs are ranked by the ATSDR as being among the top five priority hazardous substances,^1c and remember that exposures to PCBs have been found to be toxic to immunity, the liver, cartilage, and the blood brain barrier (Section 3); all of those effects may have caused long-term harm to infants born in the late 1940's and later, when exposures to PCBs increased greatly.

 

People may think that there is little reason to be concerned about airborne or parent-transported dioxins and PCBs, since it is often said that 90% of typical human exposure to those toxins is via food.  But that generalization is almost certainly based on data that is not fully representative of frequently-existing conditions:

  --  Research groups are relatively unlikely to be located in rural areas, where it would be suitable for detecting the increased dioxin absorption from rural open burning.

  --  According to the U.S. ATSDR, "PCBs are readily absorbed through the gastrointestinal tract, respiratory system and skin."^54a  

 

Chemical plant workers with higher exposures have been found  to have dioxin levels ranging as high as 2,000 pg/g lipid, whereas people in the general population with well-above-average dioxin levels (the 95th percentile) were found (in the NHANES 2003-2004 survey) to average 5.2 picograms per gram of lipid.⁵⁴  One can be confident that those 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 burning of household waste might sometimes be similar to those inhaled by the chemical plant workers.  And consider whether there is any reason not to believe that people closely exposed to backyard burning would receive very unusually high dioxin exposures.

 

As further evidence of the extent 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 about 10 times as high as those in remote areas.⁵⁵ 

 

 

Section 8:  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) 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 (vulnerability of liver to cancer, resulting from dioxins) in female rats is related to estrogens."⁵⁸

  

So it should not be surprising that, since dioxins increased in U.S. environments during the 1940's (see earlier, in Section 1), women have been more affected than men by the resulting adverse health effects, especially women who were affected during their vulnerable early developmental years (see Section 2).

 

 

Section 9: Other health declines, including sciatica: 

Adverse health effects of dioxins have been found to include bone toxicity, particularly during development, reducing bone strength.^30g,30h  And PCBs have been found to damage cartilage,^17a the tissue that, when healthy, helps prevent sciatic nerves from being pinched.  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, bear in mind that dioxin exposure has been found to be toxic to bone strength and to increase susceptibility to micro-fracture.(p. 66 of ⁶¹)

 

The above could help explain the increases in sciatica in recent decades, as reported by Case and Deaton 2017, Figure 1.13^1d).  And, combined with knowledge about greater exposures to dioxins and PCBs among people without a college degree (see Appendix I ), it could explain why sciatica has increased mainly among those with less than a BA

 

For more evidence about bone toxicity of dioxins (based on many studies), and discussion of micro-fractures (very possibly resulting from dioxin exposures) occurring in the lower back, see Appendix J.

 

 

Section 10:  Other types of pain resulting from combined effects of dioxins and PCBs:

 

Developing children would often have been exposed to both dioxins and PCBs during a period relevant to the recent midlife health downturns (see Section 1).  Those two toxins can apparently have especially serious effects when a subject is exposed to both, which is typically the case; according to the former chairman of the Canadian Institute of Child Health, 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  Any or all of those effects, which could result from combined exposures to dioxins and PCBs,  would be likely to lead to use of pain-relieving drugs or alcohol, including possibly fatal misuse.

 

So the reader should remember from Section 3 that developing infants are commonly exposed to both dioxins and PCBs in doses that have been determined to be scores to hundreds of times established safe levels when those toxins are considered separately.  But actual exposures are likely to be to both toxins at about the same time, and combined exposures apparently can have far greater effects than exposures to each of those toxins individually.

 

 

 

Conclusion:

This article has suggested that household burning of plastics-containing trash (emitting dangerous levels of dioxins) and the former widespread use of PCB-containing materials (leading to close personal exposures) merit close attention as possible causes of health declines and mortality increases.  The mid-20th-century explosive increase in use of disposable plastics²² led to major dioxin emissions resulting from rural household or farm burning of plastics,^23a which in turn led to intakes of dioxins by infants at hazardous levels (see in Section 3) during vulnerable stages of development (Section 2).  Exposures of developing children to PCBs in concentrations hundreds of times levels that are currently considered safe by the EPA (Section 3), also increased greatly in the late 1940's (Section 1).  Both of these toxins are known to have effects (Section 3) that may have led to the increasing mid-life health problems and mortality observed in later decades.  Exposures to both dioxins and PCBs would have been much greater in the U.S. than in the comparison countries (Sections 4 and 5), which is in line with differences in health and mortality data observed by Case and Deaton.  Similarly, exposures would have been much greater to both toxins for white, working-class families than for minorities or for children of college-degree-pursuing families (Appendices H and I).  Low population density is usually good for predicting where health declines and mortality increases will be greatest, because household burning of trash (with high emissions of dioxins) normally takes place only in areas of low population density; but accuracy of predicting health declines and mortality is greatly increased by taking into consideration other recognized causes of variations in dioxin exposures. (Section 6)

 

Exposures to both dioxins and PCBs increased for decades and have subsequently declined, but both of those toxins are considered to be "persistent" for good reason and are still present at hazardous levels in U.S. and other environments. (See Section 3 about dioxins; a 2010 publication of the Oregon Department of Environmental Quality made an appropriate statement about PCBs in this regard.⁷⁴)

 

Perhaps there is a lesson to be learned about the responsibilities of technological leadership, based on what transpired following wide distribution and use of plastics and PCBs in the late 1940's in the U.S.:  When preparing to introduce new products that might conceivably end up releasing chemicals with which we don't already have several decades of experience, extreme caution should be exercised to anticipate all potentially adverse outcomes.  Thorough testing should be carried out on all substances that might be anticipated to eventually end up in the environment as a result of wide distribution of the new products and materials.

 

 

 

 

*­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 dm@pollutionaction.org.  I will quickly correct anything found to be inaccurate.

 

For a more complete statement about the author and Pollution Action, please go to www.pollutionaction.org. 

 

Don Meulenberg

Pollution Action

Shenandoah, VA, USA

 

 

 

  

References:

 

1) Project TENDR: Targeting Environmental Neuro-Developmental Risks, The TENDR Consensus Statement, Environ Health Perspect. 2016 Jul; 124(7): A118–A122. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4937840/

 

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 http://www.who.int/ipcs/features/ehc_children.pdf?ua=1

 

1c) ATSDR's Substance Priority List, at https://www.atsdr.cdc.gov/spl/

1d) Case and Deaton, Mortality and morbidity in the 21st century (Final post-conference version), May 2017, at https://www.brookings.edu/wp-content/uploads/2017/03/casedeaton_sp17_finaldraft.pdf

 

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, and Table 1.14, at

http://monographs.iarc.fr/ENG/Monographs/vol107/mono107.pdf

 

1f)  MacIntosh et al., Mitigation of building-related polychlorinated biphenyls in indoor air of a school, Environ Health. 2012; 11: 24, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3353159/

 

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 http://www.nap.edu/openbook.php?record_id=2126&page=43

 

2) WHO: Don’t pollute my future!  The Impact of The Environment on Children’s Health, pp. 22 and 11, at http://apps.who.int/iris/bitstream/10665/254678/1/WHO-FWC-IHE-17.01-eng.pdf?ua=1

 

2a) WHO: Summary of Principles for Evaluating Health Risks in Children Associated with Exposure to Chemicals, p. 20, at http://www.who.int/ceh/health_risk_children.pdf?ua=1     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)

 

2b) ATSDR dioxin document, Toxicological Profile for Chlorinated Dibenzo-p-Dioxins, 1998, pp. 313 and 345, at https://www.atsdr.cdc.gov/toxprofiles/tp104.pdf

 

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 http://onlinelibrary.wiley.com/doi/10.1111/j.1742-7843.2007.00114.x/full

 

4) UMassAmherst, Environmental Health and Safety:  Polychlorinated Biphenyls (PCBs) - Hazardous Building Materials, at https://ehs.umass.edu/polychlorinated-biphenyls-pcbs-hazardous-building-materials

 

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 http://ec.europa.eu/environment/integration/research/newsalert/pdf/building_materials_used_1950_1980_in_europe_may_contribute_to_pcb_air_pollution_453na2_en.pdf

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

gov/pcbs/polychlorinated-biphenyls-pcbs-building-materials_.html#Information-Contractors

 

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

gov/sites/production/files/2016-03/documents/pcbs_in_building_materials_questions_and_answers.pdf

6) USGS:  Field Manual of Wildlife Diseases: Birds, Ch. 41, p. 303, at https://www.nwhc.usgs.gov/publications/field_manual/chapter_41.pdf

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 https://www.nap.edu/read/10041/chapter/4#27

 

8a) State of Connecticut Department of Energy and Environmental Protection:  PCB Program document at http://www.ct.gov/deep/cwp/view.asp?a=2710&q=324246&deepNav_GID=1638   

    Also Texas Dept. of State Health Services document at http://dshs.texas.gov/WorkArea/linkit.aspx?LinkIdentifier=id&ItemID=20304, p. 3

 

8b) WHO: Air Quality Guidelines, 2nd Edition, 2000, Ch. 5.10: PCBs, at http://www.euro.who.int/__data/assets/pdf_file/0016/123064/AQG2ndEd_5_10PCBs.PDF

8c) Residential Roofing Products Guide, Legends Roofing Co., at  www.legendsco.com/article1.htm

 

8d)  The 3 Most Popular Roofing Materials in Australia, at http://www.arm.net.au/the-3-most-popular-roofing-materials-in-australia/

   See also web page at www.build.com.au/roof-shingles, indicating that asphalt shingles may be hard to find in Australia

 

8e) Barbour blog:  Pros & cons of popular roofing materials, Oct 2014  at https://www.barbourproductsearch.info/pros-cons-of-popular-roofing-materials-blog000153.html

    Also, Asphalt Shingles:  Why are they so popular? at http://peakroofing.ca/asphalt-shingles-why-are-they-so-popular/

 

8f) p. 2 of EPA:  EPA/600/R-11/156 October 2011 Laboratory Study of Polychlorinated Biphenyl (PCB) Contamination and Mitigation in Buildings, at https://clu-in.org/download/contaminantfocus/pcb/PCB-lab-studies-1.pdf

 

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

at http://www.oregon.gov/deq/FilterDocs/ph-SourcePCBs.pdf

 

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

Roofing question, at https://www.thelocal.se/discuss/index.php?s=67061859aef646818aaff86fcaa05c1b&showtopic=51513&st=0&p=749542&#entry749542

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 https://kiedit.ki.se/sites/default/files/nordpcb-92.pdf   "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 https://books.google.com/books?id=g9i7AiYR8GsC&sitesec=buy&source=gbs_vpt_read  

 

11) Derek Thompson, The 33 Whitest Jobs in America, The Atlantic, Nov 6, 2013 at https://www.theatlantic.com/business/archive/2013/11/the-33-whitest-jobs-in-america/281180/

 

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

www.oregon.gov/deq/FilterDocs/HumanHealthRiskAssessmentGuidance.pdf

 

11b) EPA:  Biomonitoring / Polychlorinated Biphenyls (PCBs):  America's Children and the Environment, 3rd Ed., at https://www.epa.gov/sites/production/files/2015-05/documents/biomonitoring-pcbs.pdf

 

11c) The Surgeon General’s Call to Action to Support Breastfeeding 2011,   U.S. Public Health Service, Table 2,  at www.surgeongeneral.gov/topics/breastfeeding/calltoactiontosupportbreastfeeding.pdf,

 

12) World Bank data at https://data.worldbank.org/indicator/SP.POP.TOTL

13) ATSDR web page on polychlorinated biphenyls PCBs) at https://www.atsdr.cdc.gov/csem/csem.asp?csem=30&po=10)

Also see p. 2 of EPA:  Laboratory Study of Polychlorinated Biphenyl (PCB) Contamination and Mitigation in Buildings, at https://clu-in.org/download/contaminantfocus/pcb/PCB-lab-studies-1.pdf

 

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 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854723/

 

14a) Mosely, Reconceptualising Pain According to Modern Pain Science, Body in  Mind, Oxford Centre for fMRI of the Brain, Oxford University, Oxford, UK, at https://bodyinmind.org/resources/ 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 http://ac.els-cdn.com/089203629090050M/1-s2.0-089203629090050M-main.pdf?_tid=5f238b74-1d4f-11e7-8a29-00000aacb35d&acdnat=1491761419_84450b69c691bfdc5ffd9534957f7940

 

16) Mayo Clinic webpage on Depression and Anxiety, at https://www.mayoclinic.org/diseases-conditions/depression/in-depth/depression-and-exercise/art-20046495

   Harvard Health Letter at https://www.health.harvard.edu/mind-and-mood/exercise-is-an-all-natural-treatment-to-fight-depression

 

17)  Mayo Clinic webpage on Back exercises in 15 minutes a day, at https://www.mayoclinic.org/healthy-lifestyle/adult-health/multimedia/back-pain/sls-20076265   Harvard Health at https://www.health.harvard. 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  https://www.sciencedirect.com/science/article/pii/S1063458412008588

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

at https://www.sciencedirect.com/science/article/pii/S1063458414003653

  

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 www.pnas.org/content/112/49/15078.full.pdf;

   also p. 41 of Case and Deaton, Mortality and morbidity in the 21st century (Final post-conference version), May 2017, at https://www.brookings.edu/wp-content/uploads/2017/03/casedeaton_sp17_finaldraft.pdf

 

18) ATSDR:  Polychlorinated Biphenyls (PCBs) Toxicity: What Are Routes of Exposure for PCBs?  at https://www.atsdr.cdc.gov/csem/csem.asp?csem=30&po=6

 

19) ATSDR: Polychlorinated Biphenyls (PCBs) Toxicity:  What Are Adverse Health Effects of PCB Exposure? at https://www.atsdr.cdc.gov/csem/csem.asp?csem=30&po=10

 

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

at https://www.nwhc.usgs.gov/publications/field_manual/chapter_41.pdf

  Also Rand Corp. document at https://www.rand.org/content/dam/rand/pubs/monograph_reports/MR1377/MR1377.appc.pdf

  Also Oregon Department of Environmental Quality, Fact Sheet: Sources of Polychlorinated Biphenyls, Table 2, at www.oregon.gov/deq/FilterDocs/ph-SourcePCBs.pdf

 

21) ATSDR dioxin document, Toxicological Profile for Chlorinated Dibenzo-p-Dioxins, 1998, pp. 379 and 391, at https://www.atsdr.cdc.gov/toxprofiles/tp104.pdf

 

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 https://www.scientificamerican.com/article/a-brief-history-of-plastic-world-conquest/

 

22a) Plastics Europe: The Compelling Facts About Plastics, Figure 1, at https://www.plasticseurope.org/application/files/2815/1689/9283/2006compelling_fact_PubJan2008.pdf

 

22b) The rapid acceptance of plastics distinctly in the U.S. and the predominant role of the U.S. in use of PCBs may have been explainable in words from an article in Encyclopedia Brittanica:   "Technological leadership passed from Britain and the European nations to the United States in the course of these wars (World Wars I and II)....  it was the United States that had the capacity to assimilate innovations and take full advantage from them at times when other countries were deficient in one or other of the vital social resources without which a brilliant invention cannot be converted into a commercial success. As with Britain in the Industrial Revolution, the technological vitality of the United States in the 20th century was demonstrated less by any particular innovations than by its ability to adopt new ideas from whatever source they come." (italics added)  Encyclopedia Brittanica article on the history of technology in the 20th Century, at https://www.britannica.com/technology/history-of-technology/The-20th-century

 

23) Tox Town: Polyvinyl Chloride (PVC), at https://toxtown.nlm.nih.gov/text_version/chemicals.php?id=84

 

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  ofmpub.epa.gov/eims/eimscomm.getfile?p_download_id=523391

 

23b) Ehrlich, The PVC Debate: A Fresh Look, at https://www.buildinggreen.com/feature/pvc-debate-fresh-look

 

23c) Biemiller, Can we safely burn used plastic objects in a domestic fireplace? MIT School of Engineering, Ask an Engineer, at https://engineering.mit.edu/engage/ask-an-engineer/can-we-safely-burn-used-plastic-objects-in-a-domestic-fireplace/

 

24) ATSDR dioxin document, Toxicological Profile for Chlorinated Dibenzo-p-Dioxins, 1998, including pp. 153, 161, 163, and 165, at https://www.atsdr.cdc.gov/toxprofiles/tp104.pdf

 

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 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566290/

 

24b) Vermont Dept. of Environmental Conservation web page on Open Burning, at http://dec.vermont.gov/air-quality/compliance/open-burning

 

24d) Website of the Borough of State College, PA, at http://www.statecollegepa.us/FAQ.aspx

 

24e) Does not regulate burning of domestic refuse resulting from "normal occupancy" on property of private residences. Pennsylvania Department of Environmental Protection web page at https://www.ccpa.net/DocumentCenter/Home/View/3154

 

24f) "Burning Issue," Lancaster Online, Dec. 12, 2006, at https://lancasteronline.com/news/burning-issue/article_da81af66-4e5b-5f75-b063-5372f2d9c293.html

 

24g) Wisconsin Dept. of Natural Resources web page, Open Burning, at https://dnr.wi.gov/topic/OpenBurning/

 

24h) Minnesota Pollution Control Agency web page at https://www.pca.state.mn.us/waste/laws-prohibiting-backyard-burning-garbage

 

24j) EPA:  An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000, EPA/600/P-03/002F November 2006, Table 1-12 (see "Ferrous metals...."  for iron and steel data), at https://cfpub.epa.gov/ncea/dioxin/recordisplay.cfm?deid=159286 ; under Downloads, choose to download the Dioxin Inventory of Sources (Optimized Report).

 

24k) The New England States' prohibitions (except for Maine and Rhode Island)­­­ of burning of household trash can be confirmed by doing a Google search for "open burning permitted in (state)," which will lead one to pages from the state governments prohibiting the practice, such as the page for Connecticut at http://www.ct.gov/deep/cwp/view.asp?a=2684&q=531238

 

24m) Open Burning in Rural Minnesota, Prepared For: Minnesota Office of Environmental Assistance, January 2005, at https://www.pca.state.mn.us/sites/default/files/MOEABurnBarrelReport.pdf

 

24n) Wisconsin Dept. of Health Services:  Outdoor Wood Boilers (Water Stoves), at https://www.dhs.wisconsin.gov/air/woodboiler.htm

 

24o)  Burning Issue, Lancaster Online, accessed May 6, 2018 at https://lancasteronline.com/news/burning-issue/article_da81af66-4e5b-5f75-b063-5372f2d9c293.html

 

24p)  State College has  population of 41,992 in 2016, compared with Centre County's 160,580 in 2015 (- Google search)

  -- Centre Hall borough ordinance prohibiting open burning of trash at http://www.centrehallborough.org/Ordinances/Chapter%207%20Amended%20-%20Allowing%20Recretional%20Fires.pdf   (population 1244 in 2016 -- city-data.com)

  -- Bellefonte borough web page indicating prohibition of open burning of trash at https://ecode360.com/14491242, item 482-30  (population 6302 in 2016  - Google search)

  -- Benner township ordinance indicating prohibition of open burning of trash at http://www.bennertownship.org/ordinances/57-Burning%20Ordin.pdf  (Population 6188 in 2016  - Google search)

  -- Ferguson township apparently does not permit open burning of trash (http://www.twp.ferguson.pa.us/index.cfm?fuseaction=content.pageDetails&id=73076&typeID=40311)  (Population 17,690 in 2016 - Google search)

  -- Harris township prohibits burning of waste (see 5-6.5 at https://ecode360.com/30336765)  (population 4,873 in 2010  - Google search)

  -- Spring township prohibits open burning of trash (http://www.springtownship.org/ordinances.html)   (population 7470 in 2010  - Google search)

  -- Halfmoon township prohibits burning of waste material "which pollutes the air."  (web page at https://ecode360.com/14732635)  (pop. 2016 in 2010  - Google search)

  -- Haines township prohibits burning of toxic materials, which presumably should include burning that releases toxins (http://www.hainestwp.org/Documents/67.%20SOLID%20WASTE.pdf).  (pop. 1564 in 2010 - Google search)

  -- Potter township apparently does not prohibit open burning. (pop. 548 in 2010 - Google search)

 

24r) The only city in Clinton County (Lock Haven -- population 9549 in 2016 - Google search) only prohibits burning of garbage, meaning "articles and materials ordinarily used for food;" burning of non-food-like waste is clearly allowed. (http://lockhavenpa.gov/wp-content/uploads/2015/01/Chapter-20-Solid-Waste.pdf, Chapter 20, part 1. 

Clinton County had a population of 39,536 in 2016  (city-data.com)

  -- The township of Logan specifically permits burning of non-recyclable paper and cardboard. (https://ecode360.com/28657519)  Population of 817 in 2010 (http://www.city-data.com/city/Logan -Pennsylvania.html) 

  --  In Porter township, an ordinance that prohibits burning of trash has been proposed (in 2009) but not enacted as of a May, 2018 online inquiry. (http://www.portertownshippa.com/files/8214/1523/0868/Ordnc_Outdoor_Furnace_.pdf )

  -- Borough of Flemington:  burning of trash was first prohibited as of 2016. (http://flemingtonboroughpa.org/home/ ,  and http://flemingtonboroughpa.org/ordinances/ , both accessed May, 2016)  This prohibition was too late to be related to mortality data being used.

  -- The borough of Renovo (one of seven boroughs in Clinton County) prohibits burning of trash (https://ecode360.com/31792484)  Population 1,234 in 2014 (http://www.city-data.com/city/Renovo-Pennsylvania.html)  

  -- The township of Lamar (one of 21 townships) prohibits burning of trash   (http://library.amlegal.com/nxt/gateway.dll/Pennsylvania/lamartwp_pa/codeofordinancesofthetownshipoflamar?)f=templates$fn=default.htm$3.0$vid=amlegal:lamartwp_pa )  Population of 562 in 2010 (http://www.city-data.com/city/Lamar -Pennsylvania.html)

  

25)  PVC.org:  The history of PVC, at www.pvc.org/en/p/history

 

26)  ATSDR:  Toxicological Profile for Chlorinated Dibenzo-P-Dioxins, p. 378, at https://www.atsdr.cdc.gov/toxprofiles/tp104.pdf

 

27) Compilation of EU Dioxin Exposure and Health Data  Task 8 – Human toxicology, UK Department of the Environment, Transport and the Regions (DETR)  at http://ec.europa.eu/environment/archives/dioxin/pdf/task8.pdf

 

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 8.6.2.4 of  International Programme on Chemical Safety, Environmental Health Criteria 140, Polychlorinated Biphenyls and Terphenyls (Second Edition), at http://www.inchem.org/documents/ehc/ehc/ehc140.htm#8.6.1.1

 

29) WHO | Dioxins and their effects on human health at  www.who.int/mediacentre/factsheets/fs225/en/

 

30) Public Health England:  Dioxins Toxicological Overview, 2008, Version 1, at https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/339481/Dioxins_Toxicological_Overview_phe_v1.pdf

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: www.ncbi.nlm.nih.gov/pubmed/3393850

 

30b) Lagergren et al., Increased risk of hepatocellular carcinoma after cholecystectomy, British Journal of Cancer volume 105, pages 154–156 (28 June 2011), at https://www.nature.com/articles/bjc2011181

 

30c) American Cancer Society webpage at https://www.cancer.org/cancer/liver-cancer/detection-diagnosis-staging/signs-symptoms.html

 

30d) American Cancer Society web page at https://www.cancer.org/cancer/liver-cancer/detection-diagnosis-staging/detection.html 

 

30e) Healthline.com web page at https://www.healthline.com/health/liver-pain

 

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 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4873562/

 

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 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2788749/

 

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 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805986/ 

 

32)  Mayo Clinic:  Porphyria, at https://www.mayoclinic.org/diseases-conditions/porphyria/symptoms-causes/syc-20356066

 

33)  Balwani and Desnick, The porphyrias: advances in diagnosis and treatment, ASH Education Program, 2012,    at http://asheducationbook.hematologylibrary.org/content/2012/1/19.full

 

34) McGraw Hill Medical:  Hematology in Clinical Practice, Chapter 14: Disorders of Porphyrin Metabolism, at http://hemonc.mhmedical.com/content.aspx?bookid=1802&sectionid=124978183 

 

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 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3094426/

 

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 http://www.epa.gov/iris/supdocs/dioxinv1sup.pdf  in section 4.3.5, at end of that section, "...the resulting RfD in standard units is 7 × 10−10 mg/kg-day."  (that is, O.7 pg of TEQ/kg-d)   In the EPA’s “Glossary of Health Effects”, RfD is defined:  “RfD (oral reference dose): An estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure of a chemical to the human population (including sensitive subpopulations) that is likely to be without risk of deleterious noncancer effects during a lifetime.”

 

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)  http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download

 

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 https://cfpub.epa.gov/ncea/iris/iris_documents/documents/supdocs/dioxinv1sup.pdf (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 https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/j.efsa.2015.4124

or at http://www.dioxindb.de/dokumente/EFSA_15-05-28.pdf 

   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 ofmpub.epa.gov/eims/eimscomm.getfile?p_download_id=496304

   And another record of the EPA RfD of 0.7pgTEQ/kg bw/day is at https://www.chemistryworld.com/news/epa-sets-safe-dioxin-level/3001482.article

 

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 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240886/

 

37b) European Food Safety Authority:  Scientific statement on the health-based guidance values for dioxins and dioxin-like PCBs, May 2015, at https://efsa.onlinelibrary.wiley.com/doi/epdf/10.2903/j.efsa.2015.4124

 

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 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566290/pdf/envhper00506-0073.pdf

 

38a) See the early paragraphs of www.breastfeeding-toxins.info, citing peer-reviewed studies. 

 

38b)  ATSDR:  Polychlorinated Biphenyls (PCBs) Toxicity:  What Are Adverse Health Effects of PCB Exposure? at https://www.atsdr.cdc.gov/csem/csem.asp?csem=30&po=10

 

38c)  EPA web page on Polychlorinated biphenyls (PCBs) at https://www.epa.gov/pcbs/learn-about-polychlorinated-biphenyls-pcbs

 

38d) Oregon Department of Environmental Quality Environmental Cleanup Program, Oct. 2010, 10-LQ-023, p. D2-4 (attachment 2 of Appendix D, near very end) at

www.oregon.gov/deq/FilterDocs/HumanHealthRiskAssessmentGuidance.pdf

 

38e) CDC: Biomonitoring Summary:  Non-Dioxin-Like Polychlorinated Biphenyls, at https://www.cdc.gov/biomonitoring/NDL-PCBs_BiomonitoringSummary.html

 

38f) UNEP: Results of the global survey on concentrations in human milk of persistent organic pollutants by the United Nations Environment Programme and the World Health Organization, Geneva, 2013, p. 20, at www.pops.int/TheConvention/ConferenceoftheParties/Meetings/COP6/tabid/3074/cti/Download/mid/9701/Default.aspx?id-85&ObjID=16190  At that page, scroll down about 30 items to the title of this document.

 

39) The EPA has fluctuated in its published statements dealing with this RfD for dioxin; there may be pressures from influential people or groups (foods manufacturers have been mentioned in this regard) to avoid indicating that a safe level for dioxin is very low. Although the EPA itself may not currently publicize this RfD for cancer effects, 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 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566290/pdf/envhper00506-0073.pdf

 

  -- European Commission Environment and U.K. Dept. of the Environment, Compilation of EU Dioxin Exposure and Health Data Task 8 – Human toxicology, 1999, pp. 10, 11, at http://ec.europa.eu/environment/archives/dioxin/pdf/task8.pdf

 

  -- European Commission:  Research & Innovation, Success Stories, Dioxin risk assessment, 26 Feb. 2004, at http://ec.europa.eu/research/infocentre/export/success/article_690_en.html  

  

  -- 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 http://www.mfe.govt.nz/sites/default/files/dioxin-evaluation-feb01.pdf

  -- 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 https://www.nap.edu/read/11688/chapter/8#130

  -- 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 (see below), from the Chairman and Co-Chair of the EPA's Ad Hoc Dioxin Panel

at https://nepis.epa.gov/Exe/ZyNET.exe/P100L4AU.txt?ZyActionD=ZyDocument&Client=EPA&Index=1986%20Thru%201990&Docs=&Query=&Time=&EndTime=&SearchMethod=1&TocRestrict=n&Toc=&TocEntry=&QField=&QFieldYear=&QFieldMonth=&QFieldDay=&UseQField=&IntQFieldOp=0&ExtQFieldOp=0&XmlQuery=&File=D%3A%5CZYFILES%5CINDEX%20DATA%5C86THRU90%5CTXT%5C00000031%5CP100L4AU.txt&User=ANONYMOUS&Password=anonymous&SortMethod=h%7C-&MaximumDocuments=1&FuzzyDegree=0&ImageQuality=r75g8/r75g8/x150y150g16/i425&Display=hpfr&DefSeekPage=x&SearchBack=ZyActionL&Back=ZyActionS&BackDesc=Results%20page&MaximumPages=1&ZyEntry=3

 

 

 

40) EPA:  An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000, EPA/600/P-03/002F November 2006, Table 1-12, at https://cfpub.epa.gov/ncea/dioxin/recordisplay.cfm?deid=159286 ; under Downloads, choose to download the Dioxin Inventory of Sources (Optimized Report).

 

40a) At the EPA "An Inventory of Sources...." listed above, see p. xliv and Section 6.5, "Backyard Barrel Burning."

 

40b) The author of this article, observing from a residence on a hill in a small Virginia town, has observed open burning often taking place without use of a barrel, just in an open area in a backyard.

 

40c) Tox Town: Polyvinyl Chloride (PVC), at https://toxtown.nlm.nih.gov/text_version/chemicals.php?id=84

 

41) New York Times:  In Rural Areas, the Heat Is on Over Practice of Trash Burning, By Lisa W. Foderaro, MARCH 7, 2005 , at https://www.nytimes.com/2005/03/07/nyregion/in-rural-areas-the-heat-is-on-over-practice-of-trash-burning.html?pagewanted=all

 

43)  Lemieux, Evaluation of Emissions from the Open Burning of Household Waste in Barrels, Project Summary, EPA/600/SR-97/134, Table 3, at  https://nepis.epa.gov/Exe/ZyNET.exe/P1003CKZ.TXT?ZyActionD=ZyDocument&Client=EPA&Index=1995+Thru+1999&Docs=&Query=&Time=&EndTime=&SearchMethod=1&TocRestrict=n&Toc=&TocEntry=&QField=&QFieldYear=&QFieldMonth=&QFieldDay=&IntQFieldOp=0&ExtQFieldOp=0&XmlQuery=&File=D%3A%5Czyfiles%5CIndex%20Data%5C95thru99%5CTxt%5C00000023%5CP1003CKZ.txt&User=ANONYMOUS&Password=anonymous&SortMethod=h%7C-&MaximumDocuments=1&FuzzyDegree=0&ImageQuality=r75g8/r75g8/x150y150g16/i425&Display=hpfr&DefSeekPage=x&SearchBack=ZyActionL&Back=ZyActionS&BackDesc=Results%20page&MaximumPages=1&ZyEntry=1&SeekPage=x&ZyPURL

 

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

https://vinylplus.eu/uploads/Modules/Documents/understanding_the_basics_dioxins.pdf 

 

45) EPA web page, Agriculture: Agriculture and Air Quality: Backyard burning, at https://www.epa.gov/agriculture/agriculture-agriculture-and-air-quality#backyardburn

  

47) USDA web page "Hispanic Farmers" at https://www.agcensus.usda.gov/Publications/2012/Online_Resources/Highlights/Hispanic_Farmers/Highlights_Hispanic_Farmers.pdf

 

48) U.S. Census Bureau, Overview of Race and Hispanic Origin: 2010, at https://www.census.gov/content/dam/Census/library/publications/2011/dec/c2010br-02.pdf

 

49) USDA:  Black Farmers, at https://www.agcensus.usda.gov/Publications/2012/Online_Resources/Highlights/Black_Farmers/Highlights_Black_Farmers.pdf

50) U.S. Census Bureau Quick Facts at https://www.census.gov/quickfacts/fact/table/US/PST045216

 

50a) USDA:  The Changing Organization of U.S. Farming, 2011, pp. 7-8, at http://www.ncga.com/upload/files/documents/pdf/changing_structure_of_us_farms_usda_ers.pdf.

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 https://www.census.gov/newsroom/cspan/1940census/CSPAN_1940slides.pdf

 

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 http://ehsdiv.sph.berkeley.edu/holland/publications/files/Weldon2011.pdf 

 

52) U.S. ATSDR, Toxicological Profile for Chlorinated Dibenzo-P-Dioxins, p. 404, at http://www.seagrant.umn.edu/water/report/chemicalsofconcern/dioxins/dioxins.pdf

 

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 https://www.cdc.gov/biomonitoring/DioxinLikeChemicals_BiomonitoringSummary.html

 

54a) P. 411 of U.S. ATSDR:  Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000 at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf  Also  p. 179 of U.S. ATSDR, Persistent chemicals found in breast milk, Appendix A, at https://www.atsdr.cdc.gov/interactionprofiles/ip-breastmilk/ip03-a.pdf  "...studies of humans and animals exposed to airborne PCBs provide qualitative information that inhaled PCBs can be absorbed (ATSDR 2000).

 

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 https://cfpub.epa.gov/ncea/dioxin/recordisplay.cfm?deid=87726

 

55a) 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 smoke from a household's burning in low-density areas,

-- there would be fewer neighbors who could contribute to an unhealthful total local level of smoke pollution,

-- 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,

-- any affected neighbors would have difficulty finding other bothered neighbors with whom they could band together in complaining, especially since most people in such areas engage in the practice,

-- local governments are much less likely to prohibit open burning in low-density areas, since most of their constituents want to continue doing such burning.

 

55b) Population Reference Bureau:  Census Bureau to Track Both Metro and 'Micropolitan' Areas, June 2003, accessed April 26, 2018, at https://www.prb.org/censusbureautotrackbothmetroandmicropolitanareas/

 

55d) CDC: 2013 NCHS Urban–Rural Classification Scheme for Counties, at https://www.cdc.gov/nchs/data/series/sr_02/sr02_166.pdf

 

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 https://www.epa.gov/sites/production/files/2013-09/documents/tefs-draft-052808-0804.pdf

 

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

at https://www.theatlantic.com/education/archive/2017/09/the-rural-higher-education-crisis/541188

 

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 https://www.nap.edu/read/11688/chapter/8#117

 

59) CDC: Biomonitoring Summary: Dioxin-Like Chemicals: Polychlorinated Dibenzo-p-dioxins, Polychlorinated Dibenzofurans, and Coplanar and Mono-ortho-substituted Polychlorinated Biphenyls  at https://www.cdc.gov/biomonitoring/DioxinLikeChemicals_BiomonitoringSummary.html

61) Finnila, Bone Toxicity of Persistent Organic Pollutants, dissertation presented at University of Oulu, Finland, 2017, at http://jultika.oulu.fi/files/isbn9789526205090.pdf  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 https://www.sciencedirect.com/science/article/pii/S2255497115001706

63) Finnila et al., Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure on bone material properties, Journal of Biomechanics, Apr 2010, at https://www.ncbi.nlm.nih.gov/pubmed/20132933

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 https://www.ncbi.nlm.nih.gov/pubmed/18835322

65) L. Gallagher, High-resolution 'laser x-rays' could spot tiny fractures in bone, Imperial College of London, Aug. 2015, at https://www.imperial.ac.uk/news/167166/high-resolution-aposlaser-x-rays-could-spot-tiny

66) Jarraya et al., Review Article::Radiographically Occult and Subtle Fractures: A Pictorial Review, Radiology Research and Practice, Volume 2013 (2013), at https://www.hindawi.com/journals/rrp/2013/370169/

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 http://www.jstor.org/stable/40965865

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 https://onlinelibrary.wiley.com/doi/full/10.1359/jbmr.2001.16.10.1812­­­­

70) Jayson, Difficult diagnoses in back pain, British Medical Journal Volume 288 10 March 1984, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1444656/pdf/bmjcred00491-0010.pdf

71) Healthline web page on Alcoholic Hepatitis at https://www.healthline.com/health/alcoholic-hepatitis#diagnosis

 

72) Case and Deaton (2017, p. 19)^1d write 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." 

 

73) Hadland et al. (CDC):  Alcohol Policies and Alcoholic Cirrhosis Mortality in the United States, Original Research — Volume 12 — October 15, 2015 at https://www.cdc.gov/pcd/issues/2015/15_0200.htm

--  Also Walsh and Alexander, Review:  Alcoholic liver disease, BMJ Postgraduate Medical Journal, at http://pmj.bmj.com/content/76/895/280.

"Alcohol is 'a' major cause of liver cirrhosis."

 

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

www.oregon.gov/deq/FilterDocs/HumanHealthRiskAssessmentGuidance.pdf

 

 

 

 

 

Appendix A:  Additional evidence related to turns for the worse taking place among Americans born during the 1940's, especially those born after 1945, when dioxin and PCB exposures increased in the U.S.

 

Remember from Section 1 the exposures to dioxins and PCBs that were minor early in the 1940's, but which increased especially after 1945, in the cases of both toxins.  Dioxin exposures would have increased especially in 1947 and later when disposable plastics, production of which increased dramatically after 1945, started to be widely burned in backyards and incinerators.  Extra increases of PCB exposures would have begun in 1949 when those chemicals 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:

  Fig. 15

 

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, with a sign of a beginning upturn in 2007, when the 60-year-olds would have been born in 1947.

  -- Among 55-year-olds (middle chart), notice that around 2004, when that age group would have been born in 1949, 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. 

 

 

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 less rapid among U.S. whites than among people in almost all of the comparison countries.

 Fig. 16

 

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 plastics were becoming ever more widespread and 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 an area that is too complicated to deal with in this article, but which is dealt with in detail in www.pollution-effects.info/. 

 

 

Appendix B:  More on the relationship  between PCB exposures and mortality results among the countries discussed: 

 

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, extended 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. 

 

 

Appendix C:  Childhood exposures to PCBs can have effects in later life:

As mentioned in the main text, reduced immunity to disease was recognized in an expert consensus statement to be one of the effects of PCBs,³ an effect that would clearly have long-term consequences.

  

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; so long-term effects of PCBs on the blood brain barrier might well lead to felt needs for pain-relieving substances such as opioids or alcohol, or even to deaths of despair.

 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

 

 

Appendix D:  The case of Australia in relation to PCB exposures:  Australia, also, had an unfavorable trend in drug, alcohol and suicide mortality, but in Australia's case the mortality increase took place despite a relatively minimal use of asphalt roofing.^8d  However, exposures to PCBs in Australia via their uses in other applications, including as fire retardants in ceiling tiles,^8g would have been in addition to the minimal exposures from roofing materials; and all exposures combined could have resulted in more volatilization of PCBs than would normally occur in cooler climates, because of the effect of the high summer temperatures in Australia. (See (b) in Section 5)

 

 

Appendix E:  Latency of effects, especially related to cancer, with particular reference to liver cancer: 

 

 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 (see earlier);

  -- the workers who were the ones with very unexpectedly high mortality were autoclave workers, who would have had especially close exposure to chemical reactions that were probably major sources of 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 earlier)

 

Appendix F:  The case of Centre County, Pennsylvania

Fig. 12a

 --  A sole low-mortality spot can be seen in the middle of Pennsylvania,  as shown in Figure 12a on the left.  That is Centre County, which includes the borough of State College, the largest town in that county. 

 

This appears to be an exception to the normal linkage of low-mortality areas in the eastern half of the U.S. (Figure 7) with dense population (Figure  9). (The U.S. West in not useful in this discussion because many of the statistical areas are too large and imprecise to be relevant to local differences.)  As discussed earlier, the usual association between mortality and density is very likely caused by household trash burning in low-population-density areas, resulting in dioxin emissions and higher mortality; on the other hand, high population density normally leads to low burning/low dioxin emissions and therefore (probably) to reduced mortality.  But in this case it appears that local ordinances, also, can lead to low burning of trash; the borough of State College flatly prohibits open burning of trash,^24d as do most of the other towns in Centre County from which such information is available online.^24p  By contrast, the Department of Environmental Protection of the surrounding state of Pennsylvania does not have any such prohibition;^24e,24f and burning of household trash appears to be common in much or most of Pennsylvania.^24f  For comparison with burning practices in the region immediately surrounding Centre Country, we looked at Clinton County, with which Centre County shares more common border than with any other county; of the governmental entities in Clinton County that provide information online about their waste-burning-related ordinances, the units governing the overwhelming majority of the population do not prohibit burning of waste, and only a very small minority do prohibit burning of waste.^24r 

 

So there is clearly

--  a dramatic difference between permitted practice of waste burning in Centre County and what is permitted in the only adjoining county that was researched, a county that was reasonably chosen for comparison, and

--  a major difference between waste burning that is permitted in Centre County and what is permitted by and apparently practiced in the surrounding state of Pennsylvania.

   

So when we see that Centre County shows up with mortality that is conspicuously low in comparison with almost all of the rest of Pennsylvania (Figure 12a above), it would be reasonable to suggest that at least one cause of that (and very possibly the main cause) may be Centre County's distinctly low tolerance for household waste burning, a practice that is recognized to emit substantial dioxins. (See Section 3) 

 

Appendix G:  Confirmation of the link between low-population-density location and increasing mortality, with two different types of data:

 

In reporting by Case and Deaton about comparative mortality rates among six different residential classifications (p. 21 of ref. 1d), the results were compatible with what would be expected if there had been a major source of toxic exposures in rural areas that was new in the mid-20th century.  First, we need to understand how counties are assigned to the various residential classifications, according to guidelines from the U.S. Office of Management and Budget.  Most of the classifications include complete outlying counties that are linked to metropolitan areas by commuting, even if  only 25% of the workers in the outlying counties commute to the city for work;^55b therefore, in general, very substantial rural-residing population is likely to be included in all four of the less-urban residential classifications.^55d  (That would apparently apply only minimally to large metropolitan statistical areas since there is a separate classification -- large fringe MSAs -- that specifically includes the counties surrounding large central MSAs.)

 

Note in Figure 15 below how low the population densities are in the four least-urban classifications, compared with the densities in the large central metro areas -- all of those four lower densities are less than 8% as high as the average density in the large central metro areas. 

Fig. 15

 
 

If a practice (such as backyard burning) is described as basically rural, it would probably be significantly taking place in areas where the average population density is less than 8% as high as the average density in large central metro areas.  That would be especially true in the many rural counties from which as few as 25% of the residents so much as commute to a city, but which are nevertheless completely included within a "metropolitan" statistical area.^55b 

 

Case and Deaton found more favorable mortality outcomes in both of the two more-urban residential classifications, especially in the most urban category; and that was very likely related to the lower dioxin emissions within those areas, resulting from less trash burning than is typical in rural areas. The cities would have received dioxin emissions from household trash burning mainly in greatly-reduced concentrations, by way of windborne drift from less-urban areas.  And the urban-rural difference in mortality increases, very possibly resulting from urban-rural differences in dioxin-emitting trash burning, would have arisen relatively recently as a long-term effect of the dramatic 20th-century growth in use of disposable plastics.

 

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

 

 

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.

 

Effects of rural exposures to toxins:  We should remember that backyard burning, with its emissions that the EPA considers to be dangerous (see earlier), is a predominantly rural practice; 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  Summarizing, whites are over-represented among farmers compared with their percentage in the U.S. population, Hispanics are very under-represented compared with their percentage in the population, and blacks are even more under-represented in that same regard.

 

So it should not be surprising that, when a distinctly rural practice (open burning) became dangerous after its normal contents came to include plastics (see earlier), whites should have had very significant increases in mortality whereas the apparent effect was very low among black non-Hispanics and in-between among Hispanics (as recorded in Table 2 of Case and Deaton 2017).^1d.

 

The question may come up as to why so much importance is attached to practices of farmers, since many residents of areas of low population density (where mortality increases and health declines are greater) are not active farmers.  It is because many farmers would have distinctly large amounts of plastics to dispose of, since it is normal for hay purchases to arrive wrapped in plastic.  Therefore dioxin emissions from burning on farms would be expected to be very unusually high.

 

 

Alcoholic liver disease and cirrhosis mortality according to ethnicity and dioxins:

 

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 short way of saying "alcoholic liver disease and cirrhosis" mortality. (That is how 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, in Section 3); symptoms of alcoholic liver disease are similar to symptoms of other health problems,⁷¹ and there is good reason to believe that stated causes of death are often inaccurate;⁷² so the deaths attributed (in Case and Deaton 2017) to alcoholic liver disease and cirrhosis may have often actually been results of non-alcohol-related liver damage, such as is known to be caused by dioxin exposures.  (Less than half of all cirrhosis mortality in the U.S. is linked to alcohol consumption.⁷³)  Backyard burning is known to the EPA to be a major source of dioxin emissions, and that source is one to which people are exposed in "particularly dangerous" concentrations (see earlier); it is basically a rural practice, to which farm families (who are very disproportionately white) would be heavily exposed, and to which black and Hispanic families would have only minimal exposure. (See earlier in this Appendix.) 

 

Even when the deaths were correctly attributed to alcohol, it is entirely possible that resorting to excessive alcohol may have been a way of responding to pain that resulted from harm, possibly including non-alcoholic liver damage, of kinds known to be caused by dioxins. (See earlier)

 

The above may help explain why families of non-Hispanic whites, with their high exposures to dioxin emissions as trash-burning farm families, were disproportionately affected by the mortality increases that have been reported by Case and Deaton.

 

It should be remembered that people could be exposed to these toxins during sensitive, vulnerable periods of early child development (see earlier); dioxin concentrations to which average infants are exposed (according to an EPA research team) greatly exceed authoritatively-established safe levels (see earlier).

  

Exposures to PCBs, in non-rural areas:  Remember (from Section 1) that mid-century was the time of rapid increase of children developing who would later be affected by despair.  Children would have been exposed to PCBs that were increasing in the environment after 1945 and that were being emitted by building materials that were first used in 1949 and later (see earlier, in Section 1).  Those most exposed would have been

   a) children living or going to school in recently-built buildings, or

   b) children exposed via parents who had exposures to recently-built buildings (including residences);

 

the above in turn would have been more likely for the economically-favored ethnic group (non-Hispanic whites) compared with disadvantaged minorities.

 

PCBs would have affected mainly whites:  PCBs were used in transformers and other electrical equipment, hydraulic and heat-transfer fluids, caulk, lubricants, ⁸ insecticides,⁶ and many other industrial applications, during the mid-century-to-1970's period.⁴  An article in The Atlantic entitled "The 33 Whitest Jobs in America," listed 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 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 predominantly-white workers (and their children, indirectly^1b) would have been exposed to PCBs in materials that were part of work in those occupations in the mid-20th Century.

 

Also, 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 women^11b (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. 

 

 

 

Appendix I:  Disproportionate effects of PCBs and dioxins on children of non-degree-pursuing families:

(Case and Deaton found that people without college degrees had higher rates of mortality, including deaths of despair, than college graduates)

 

PCBs:  College graduates would very seldom go into the trades that have had major contact with PCBs (see the "whitest" occupations, above in Appendix H).  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. 

 

Dioxins:  Aside from increasing "deaths of despair" discussed above, Case and Deaton (2017, p. 8^1d) also point out that increasing midlife white all-cause mortality rates are particularly high for those with no more than a high school degree.  In Section 7, 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, and producing and handling pesticides and a variety of other chemicals. (Section 5.5.2 of ref. 21)  So it should be apparent that many types of workers would have occupational exposures to dioxins, and very few of those workers would be college graduates.  

 

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; families of the degree holders would typically live farther away in suburbs, better removed from the pollution.  Living closer to polluting factories would especially affect the workers'  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

 

 

Appendix J:  More evidence of bone toxicity of dioxins, especially during development:  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; 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  (More on this below)

 

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.

 

Appendix K:  Internet searches for articles about household burning of trash in the comparison countries:

 

When doing a Google search (3/30/2018) for "household 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, Canada, Australia and Romania. 

 

A search with the same search phrase on Yahoo (5/26/2018, going through 16 pages) led to two articles referring to household burning in Ireland (entitled, "Burning of Waste," discussing the "increase in reported 'backyard burning' of domestic household waste" at http://www.epa.ie/waste/burn/; "Burning of Waste:  What is Backyard Burning," saying "Many people may think that they are doing the right thing" at http://www.epa.ie/waste/householder/burn/;  a separate search (using google.uk) brought up a web page stating that "such illegal practices are the main cause of dioxins in our air in Ireland." at https://www.independent.ie/regionals/kerryman/lifestyle/a-burning-issue-30043288.html.

 

Additional web pages from the above search were about the practice in Canada ("Open Burning of Garbage:  health and environmental risks," where one can follow a link to a brochure that says, "In Canada, the open burning of garbage produces more dioxins and furans than all industrial activities combined." at https://www.canada.ca/en/environment-climate-change/services/managing-reducing-waste/municipal-solid/environment/open-burning-garbage-health-risks.html), one regarding Australia ("Can I burn household rubbish or garden waste in my backyard or acreage?" in which the article indicates that backyard burning is prohibited in certain specified areas, essentially acknowledging that it will take place outside those areas, at http://www.environment.nsw.gov.au/questions/burn-household-rubbish-garden-waste); a U.K. discussion group on the subject, in which pros and  cons of burning household trash are discussed at length, in the course of which nobody brings up the consideration that it could be illegal; so this is an in-between situation, in which it is apparent that open burning of trash is merely a matter of personal preference, but nobody reports that it actually is taking place widely, at https://www.theguardian.com/notesandqueries/query/0,5753,-26332,00.html; one article regarding open burning in Cambodia and one about it in India, as well as numerous articles about this practice in the U.S.  An international forum discussion on the topic was found at www.cbsm.com/forums/index.lasso?p=9099, in which two contributors discuss household trash burning in Australia and Canada.

 --  A search on Google.com.au (leading search engine in Australia) on 6/11/18 using the search phrase "household burning of waste in Australia" brings up a report (at http://blogs.nelson.wisc.edu/es112-302-3/waste/) stating that "many indigenous people in Australia burn their waste," (indigenous population in Australia in 2016 was almost 670,000 , according to a government source at www.abs.gov.au/ausstats/abs@.nsf/mf/3238.0.55.001), and an article at https://www.wastenot.org.au/history-of-waste/  saying that household burning of plastics-containing trash was common among Australians in some places until the early 21st century.

--  A search using google.de (which is used by about 94% of Germans) (5/27/2018, going through the first 100 listings, aided by a good working knowledge of German based on 4-1/2 years of study) yielded no articles dealing with household burning of trash as a problem in Germany or in any of the comparison countries; the search phrase used was "private Verbrennung von Abfall in Europa," which brought up the most relevant results of the variations tried.

--  A search using google.fr (used by about 93% in France) (5/27/2018, using search phrase "brulage des ordures menageres," going through the first 20 listings, making use of Google's translator) brought up many websites saying burning of waste is forbidden and one saying that it was done significantly, but in Canada.

--  A search using google.se (predominant in Sweden) (5/27/2018, going through the first 90 listings) brought up only one article about the practice being widely done in the developing world.

--  A search using google.uk (5/28/2018, first 10 pages) brought up an article about the practice in Mexico, one about it in the Cayman Islands, an extremely large number about the practice in the U.S., one UK site that could not download, and one page from GOV.UK (at https://www.gov.uk/garden-bonfires-rules) saying there is no law against burning but you can't do so "if it will cause pollution or harm people’s health."  But no reports were found about household burning actually taking place.

--  A search on google.dk using "private burning of waste in Denmark" (which worked best) brought up nothing except articles about municipal incineration, in the first 4 pages of listings.

--  A search on Google.nl (Netherlands) on 6/10/18 using the search phrase "huishoudelijk verbranden van afval" and going through the first 22 entries yielded articles about burning of trash in neighboring Belgium and many articles about municipal incineration of waste, but nothing about household burning of trash in the Netherlands.

--  A search on Google.it (Italy) on 6/10/18 using the search phrase "famiglia che brucia di spazzatura" yielded (in the first two pages of results):

   1) two news stories about outraged citizens reporting about burning of trash that included plastics but at levels apparently well below what could be described as common.  In the Google translation of one of the articles, such an activity "must be officially reported by the police because the gesture is of criminal importance,"  and the expected outcome in the other article was similar;

   2) a complaint on an online forum, the response to which made it clear that private burning of plastics-containing trash was illegal and reportable as a crime,

   3) a report about illegal dumping and burning of dumped waste at a well-known location that is apparently unusual.

 

 

 --  A search on Google.es (by far the dominant search engine in Spain, but also for Spanish-language searching) going through 2-1/2 pages on 6/10/18 using the search phrase "Quema de basura doméstica" yielded many articles about household burning of waste in Latin America, one about it in the U.S., and many error messages, but nothing about household burning of trash in Spain.

 --  A search on Google.co.jp (the dominant search engine in Japan) using the search phrase,  ゴミの家庭用燃焼 (Gomi no katei-yō nenshō) with the help of Google's translator on 6/11/2018 yielded almost nothing but error messages.

--  A search on Google.ch (Switzerland) on 6/11/18 using the search phrase "Abfallverbrennung auf privaten Grundstücken" going through two pages showed nothing but websites from Germany and Austria, and one non-relevant page from Switzerland.