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ADVERSE THYROID HEALTH EFFECTS OF COAL ASH EXPOSURE

by

Guning Liu

BM in Public Health Administration, Capital Medical University, China, 2015

Submitted to the Graduate Faculty of

the Department of Environmental and Occupational Health

Graduate School of Public Health in partial fulfillment

of the requirements for the degree of

Master of Public Health

University of Pittsburgh

2017

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UNIVERSITY OF PITTSBURGH

GRADUATE SCHOOL OF PUBLIC HEALTH

This essay is submitted

by

Guning Liu

on

June 20, 2017

and approved by

Essay Advisor:Linda L. Pearce, PhD ______________________________________Assistant ProfessorEnvironmental and Occupational HealthGraduate School of Public HealthUniversity of Pittsburgh

Essay Reader:Martha Ann Terry, PhD ______________________________________Associate ProfessorBehavioral and Community Health SciencesGraduate School of Public HealthUniversity of Pittsburgh

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Copyright © by Guning Liu

2017

ABSTRACT

Coal ash from coal burning is a stationary source of air pollution in industrial countries.

More than one-third of US electricity is generated from coal burning. Even though about 50% of

coal combustion residuals (CCR) can be reused with current technology, the disposal of coal ash

is still inevitable, potentially causing adverse health effects in both adults and children. About 12

in every 100 people experience a thyroid disorder during their lifetime. In the current US

population, 20 million people are estimated to have thyroid disorders of some kind, and fewer

than half are aware of their condition. Some thyroid diseases are hard to diagnose, and most

require regular monitoring for life. Although thyroid medication is not as expensive as cancer

treatment, thyroid disorders can still cause great economic difficulty. This essay provides an

introduction to coal ash and thyroid problems for interested members of the public. It is a

literature review with a brief discussion of whether possible correlations exist between coal ash

and thyroid disorders. It is of significant public health benefits to conduct further research in this

subject.

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Linda L. Pearce, PhD

ADVERSE THYROID HEALTH EFFECTS OF COAL ASH EXPOSURE

Guning Liu, MPH

University of Pittsburgh, 2017

TABLE OF CONTENTS

1.0 INTRODUCTION.........................................................................................................................1

2.0 BACKGROUND IN COAL ASH AND BY-PRODUCT...........................................................2

2.1 COAL ASH..........................................................................................................................2

2.2 PRODUCTION OF COAL ASH.......................................................................................3

2.3 DISPOSAL AND REUSE BENEFIT................................................................................7

2.4 RADIOACTIVE CONTAMINANTS IN COAL ASH...................................................11

2.5 HAZARD............................................................................................................................12

3.0 THYROID DISORDERS...........................................................................................................15

3.1 BIOLOGICAL PROFILE................................................................................................15

3.1.1 Thyroid disorders.......................................................................................................16

3.1.2 Hyperthyroidism.........................................................................................................16

3.1.3 Hypothyroidism..........................................................................................................17

3.1.4 Hashimoto’s Thyroiditis.............................................................................................18

3.1.5 Graves’ disease............................................................................................................19

3.1.6 Thyroid nodules..........................................................................................................19

3.2 ENVIRONMENTAL RISK FACTORS FOR AUTOIMMUNE THYROID DISEASE

(AITD) .............................................................................................................................................20

4.0 CROSS-DISCIPLINE STUDIES AND DISCUSSION............................................................22

5.0 CONCLUSION............................................................................................................................27

BIBLIOGRAPHY......................................................................................................................................30

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LIST OF TABLES

Table 1. 2010-2015 U.S. Aggregated Coal Mine Production..........................................................4

Table 2. 2015 Partial Coal Combustion Product Survey Report.....................................................9

Table 3. Radioactivity Concentration in CCR and Coal................................................................11

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LIST OF FIGURES

Figure 1. Coal Power Plants Distribution Map................................................................................5

Figure 2. 2010-2015 The US Aggregated Coal Mine Products.......................................................5

Figure 3. Coal Burn Process............................................................................................................6

Figure 4. Total CCR Production Amount and Recycle Rate...........................................................9

Figure 5. Coal Fly Ash Production and Recycle Rate.....................................................................9

Figure 6. Bottom Ash Production and Recycle Rate.......................................................................9

Figure 7. Boiler Slag Production and Recycle Rate........................................................................9

Figure 8. FGD Production and Recycle Rate................................................................................10

Figure 9. Estimates of Thyroid Cancer New Cases (2005-2017)..................................................20

Figure 10. Estimates of Thyroid Cancer Deaths (2005-2017).......................................................20

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1.0 INTRODUCTION

The significance of thyroid problems in populations can be traced back to the 1970s. Research

done by Tunbridge et al. (1977) in Whickham, County Durham, North East England, revealed

that 6.6% of the general adult population had thyroid dysfunction. Thyroid disorders present with

various symptoms. Elevated thyroid-stimulating hormone (TSH) was found in 9.5% of health

fair participants in the Colorado Thyroid Disease Prevalence Study (Canaris et al., 2000). In the

NHANES III study (Hollowell, 2002), researchers enrolled 17,353 participants to represent the

general United States (US) population. They found that 5% of the participants had

hypothyroidism, and 1.5% had hyperthyroidism.

Coal combustion residuals (CCR) disposal poses a potentially hazardous chronic

exposure. Residents near disposal sites experience severe respiratory symptoms and increased

cancer risk. Research on the health effects associated with coal ash exposure is limited so far.

Available data on coal ash include animal studies (Dogra et al., 1995; Finger et al., 2016),

exposure studies (Ruhl et al., 2009; Silva et al., 2012; Souza et al., 2013), and chemical studies

(Roessler et al., 2016). Only a few studies have focused on coal ash in the landscape. This essay

reviews research on coal ash and thyroid disorders and discusses the possible relationship

between them.

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2.0 BACKGROUND IN COAL ASH AND BY-PRODUCT

2.1 COAL ASH

Coal ash is the powdered material generated through the coal-burning process. It is stored

throughout the United States, with limited monitoring of the potential environmental and human

health impacts. Storage sites include piles, landfills, and holding ponds. The US Environmental

Protection Agency (EPA) estimates that currently open storage sites consist of 300 landfills and

584 ash ponds throughout the country.

The EPA (United States Environmental Protection Agency, 2009) reported that over six

million people live within the ‘zip code tabulation area’ around 495 electric utility plants . With

growing concern about CCR disposal, the first regulation regarding CCR was issued in 2010,

followed by the “Disposal of Coal Combustion Residuals (CCR) from Electric Utilities Final

Rule” from the EPA in 2014. A supplementation proposal regarding certain inactive CCR was

added to this rule in late 2016. The rule is based on extensive previous study and focused on the

risk factors of CCR disposal, such as leaking monitors at storage sites.

Coal ash refers to multiple products and poses a great threat to human health. Fly ash,

which is the predominant component of coal ash (up to 80%), consists of fine particles with

diameters less than 10μm. These small particles, many of which are heavy metals and radioactive

elements, are highly hazardous, because they penetrate deep into lungs, and some enter the blood

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cycle.

The age of coal ash storage sites varies considerably, but many lack protections necessary

to prevent coal ash from polluting groundwater and the air (Zierold & Sears, 2015). The current

methods of storage allow for fugitive dust emissions and infiltration into groundwater. A survey

of states with coal ash sites found that 36% did not meet requirements for landfills, 67% did not

meet coating requirements for ash ponds, 19% were without landfill groundwater monitoring,

and 61% were without pond groundwater monitoring.

Despite high-level toxicity and hazard potential, limited research has been done on the

health effects of coal ash exposure. Several studies have focused on workplace exposure, and

some have assessed prenatal and childhood exposure (Chernick et al., 2016; Bencko et al., 1980;

Bencko et al., 1988; Chen, Chen & Chia, 2010; Zierold & Sears, 2015). Workers exposed to coal

ash have increased genetic mutations and cell damage, increased frequencies of chromosome

aberrations, decreased lung function, higher malignancy mortality at younger ages, and increased

levels of transferrin, orosomucoid, and ceruloplasmin (Chen, Chen & Chia, 2010; Zierold &

Sears, 2015). Chinese children exposed to coal ash containing polycyclic aromatic hydrocarbons

during the prenatal period had decreased neurology and cerebrum development, in turn affecting

language and social skills (Liang et al., 2010; Tang et al., 2008).

2.2 PRODUCTION OF COAL ASH

Coal ash is the by-product of coal-fired electric power plants. There is rarely an industry that

produces coal ash as its purpose. When mentioning coal ash, most people refer to the residuals of

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coal burning in power plants, or CCR. CCR consists of several different compounds, including

fly ash, bottom ash, boiler slag, and flue gas desulfurization material. Although cleaner and more

environmentally friendly methods to generate electricity exist (nuclear energy and solar

production, for example), most are expensive and require sophisticated technology compared to

coal-burning power plants. So, coal burning is still the primary source of electricity in the US,

accounting for about 45% of electricity output. The US has about 28% of global coal reserves,

which is approximately 477 billion short tons. Seven hundred and seventy-four million short tons

of coal were used in electric power plants in 2015, as reported by the Energy Information

Administration (EIA).

The ‘required level of coal’ is the estimated amount of coal needed for electricity

production and other industrial use. According to the EIA and the EPA, in 2016, the total coal

required level remained the same as in 2015, even though several major power plants closed.

Most coal power plants are located in Kentucky, West Virginia, Pennsylvania, and Indiana

(Figure 1). There was a total of 896,940,563 short tons of coal mine production in the US in

2015 (Table 1). Over the years, we can observe a mild decreasing trend in the coal mine industry

(Figure 2). This information was collected by EIA.

Table 1. 2010-2015 U.S. Aggregated Coal Mine Production

2010 2011 2012 2013 2014 2015

United States Total 1,084,368,148 1,095,627,536 1,016,458,418 984,841,779 1,000,048,758 896,940,563Middle Atlantic 58,593,111 59,181,827 54,718,802 54,008,748 60,909,704 50,030,833

Pennsylvania 58,593,111 59,181,827 54,718,802 54,008,748 60,909,704 50,030,833East North Central 94,897,917 103,361,794 111,533,858 116,361,864 119,488,642 107,437,449

Illinois 33,241,392 37,770,397 48,486,048 52,147,193 57,969,300 56,101,030Indiana 34,949,969 37,425,683 36,720,174 39,101,834 39,266,977 34,295,444Ohio 26,706,556 28,165,714 26,327,636 25,112,837 22,252,365 17,040,975

West North Central 29,540,112 28,733,414 27,966,117 28,074,913 29,586,372 29,139,23

1Kansas 132,691 37,257 15,864 22,150 66,366 199,199Missouri 458,477 464,738 412,587 413,703 362,813 138,206

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North Dakoda 28,948,944 28,231,419 27,528,666 27,639,060 29,157,193 28,801,826

South Atlantic 160,190,307 160,121,171 141,673,204 131,330,650 129,224,479 111,469,038Maryland 2,585,156 2,936,758 2,283,341 1,925,291 1,977,928 1,921,869Virginia 22,385,402 22,522,668 18,965,105 16,619,072 15,059,178 13,914,269West Virginia 135,219,749 134,661,745 120,424,758 112,786,287 112,187,373 95,632,900

East South Central 130,658,741 132,130,979 114,226,008 103,673,302 98,274,017 78,656,669(Table 1 Continued)

Alabama 19,914,940 19,071,050 19,312,139 18,620,017 16,362,945 13,190,832Kentucky 104,960,118 108,766,150 90,861,804 80,379,779 77,334,723 61,424,961Mississippi 4,003,505 2,746,744 2,952,818 3,575,069 3,737,100 3,143,392Tennessee 1,780,178 1,547,035 1,090,247 1,098,437 839,249 897,484

West South Central 45,969,255 51,046,309 49,301,448 46,854,765 47,257,201 40,228,355

Arkansas 32,301 133,347 98,121 58,578 93,989 91,462Louisiana 3,944,542 3,864,700 3,971,129 2,809,771 2,604,888 3,438,728Oklahoma 1,010,411 1,144,665 1,053,973 1,135,797 904,311 780,199Texas 40,982,001 45,903,597 44,178,225 42,850,619 43,654,013 35,917,966

Mountain 560,510,879 557,252,677 513,663,157 500,939,684 512,182,976 477,417,852Arizona 7,752,277 8,110,942 7,493,276 7,602,722 8,050,607 6,804,555Colorado 25,162,526 26,889,632 28,566,094 24,236,286 24,007,495 18,878,915Montana 44,732,165 42,008,238 36,693,982 42,231,483 44,562,048 41,864,004New Mexico 20,990,588 21,922,457 22,452,275 21,968,641 21,963,311 19,678,796Utah 19,350,951 19,648,020 17,015,919 16,976,724 17,934,416 14,419,078Wyoming 431,106,631 442,522,372 438,673,388 401,441,611 387,923,828 375,772,504

Pacific Non-Contiguous 2,151,094 2,148,926 2,052,086 1,631,584 1,501,758 1,177,390

Alaska 2,151,094 2,148,926 2,052,086 1,631,584 1,501,758 1,177,390(Table created by author from data collected by the US EIA [June 12, 2017] )

Figure 1. Coal Power Plants Distribution Map (Figure source: US EIA [June 12, 2017])

Figure 2. 2010-2015 The US Aggregated Coal Mine Products (Figure created by author from data collected by the US EIA

[June 12, 2017])

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In the coal plant process (Figure 3), coal material is first burned in a boiler or furnace.

Ash particles that are too large and cumbersome to be carried through the air into the precipitator

are separated from the rest of the material. This product of the coal combustion is named bottom

ash. Then, the rest of the coal material is processed in a precipitator. Fly ash and boiler slag are

collected at the end of this process. Fly ash is a fine powdered material made mainly of silicon

dioxide, aluminum oxide, and calcium oxide. The majority of CCR is fly ash. Flue gas

desulfurization material is generated in the final step before releasing flue gas into the

atmosphere.

Standards to classify coal fly ash have been defined by the American Society for Testing

and Materials International (ASTM) C618. The standard is based on the amount of calcium,

silica, alumina, and iron in fly ash. Two classes of fly ash are defined in C618: Class C and Class

F. Not all coal ash is under classified under C618. The carbon content in coal ash is measured by

the Loss on Ignition (LOI). Only fly ash with 75% of particles no larger than 45 m and with

LOI less than 4% is classified under C618. The US standard of LOI is 6%. The use of coal ash in

different recycling categories depends its LOI. For example, only fly ash with low LOI can be

used to replace cement in concrete products. However, fly ash with high LOI can be used to

replace sand in concrete products.

Figure 3. Coal Burn Process

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(Figure created by author, source: Bencko et al., 1980)

2.3 DISPOSAL AND REUSE BENEFIT

Several devices can be used to collect coal fly ash, including electrostatic precipitators,

baghouses, cyclones, and wet scrubbers (Sahoo et al., 2016). After collection, part of CCR can

be reused to reduce environmental damage and produce economic benefits, and the rest of CCR

is usually disposed of. There are two types of disposal units for CCR. One of them is

impoundment: CCR is mixed with water and shipped to a nearby impoundment for disposal.

Another method is storage at a landfill. When disposing of coal ash in a landfill, no water

mixture is needed. The landfill is usually not close to the power plant, so coal ash needs to be

transported by ship or truck. This often costs slightly more than impoundment. Compared to

disposal, recycling is a more beneficial way to deal with CCR in the US. Several methods and

technologies have been developed, many of which are focused on the reuse of fly ash.

Part of fly ash is used in concrete products, such as asphalt concrete. Fly ash can be used

as mineral filler in asphalt paving applications. Low levels of fly ash in asphalt mixtures exhibit

features that are comparable to natural fillers. Further, coal fly ash can increase the anti-stripping

properties of asphalt (Yao et al., 2015). This means that coal ash can act as an adhesion promoter

to help prevent asphalt pavement from undergoing stripping phenomena, such as fatigue cracks

and core holes in roads.

Fly ash has also been used in structural fills for construction projects such as highway

and dam construction (Yao et al., 2015). Other types of fly ash such as lignite or sub-bituminous

are not very suitable for structural fill, because they will harden prematurely in high humidity

and potentially create handling and compaction problems. The utilization of coal ash in

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construction can lower both the cost of a building project and the processing cost of electricity

companies. In Pittsburgh, Pennsylvania, over 350,000 tons of fly ash were used in this way in

2010, and estimated economic benefits reached $860,000. However, there are some

disadvantages to this method. Because fly ash is dust material, dust control measures are needed

during the material delivery. When mixing coal ash with other construction material, erosion

control measures are also critical to the final product. Other products that can be made with

recycled fly ash include cement, flowable fill, road base, and gypsum panel products.

According to American Coal Ash Association survey results in 2015 (ACAA survey

results, 2000-2015), a total of 11,289,432 short tons of CCR were produced, and 61,053,908

short tons – approximately 52% of total output – were reused. Thirty percent of the reused CCR

is fly ash material, and it is mainly used as concrete or related products (Table 2). Based on a

survey report from the EIA, concrete products have been the major recycled CCR products over

the years, and the overall CCR reuse rate has been gradually increasing since 2000 (Figures 4-8).

The fly ash reused in concrete products rose from 13.1 million tons to 15.7 million tons over the

course of 2015. Enhanced government regulation, changes in industrial companies’ strategies,

and advanced technology are contributing factors to this increase. In correspondence with a

decrease in the actual amount of coal mining, coal ash declined slightly in 2015, but the

recycling rate increased by 4%. In a document produced by the ACAA, the reasons for the drop

in boiler slag production was noted: more power plants that produce this material were retired,

and the remaining boiler slag was mostly utilized in roofing.

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Table 2. 2015 Partial Coal Combustion Product Survey Report

Categories Fly ash Bottom ash Boiler slag FGD material Total CCRConcrete products 15,737,238 570,092 33,290 0 16,749,754Blended cement 3,629,151 1,130,802 0 0 6,409,887

Structural fills/embankments 1,277,356 1,561,531 305,770 0 4,467,462Flowable fill 107,263 9,106 0 0 116,369Road base 178,281 311,779 21 0 490,081

Gypsum panel product/wallboard 0 28,378 0 973,785 12,324,178Mining Applications 1,128,682 73,416 0 215,974 13,819,113Total CCR produced 44,365,587 12,010,425 2,228,205 12,625,907 117,289,432

Total CCR reused 24,062,786 4,819,205 1,866,912 1,502,287 61,053,908Recycle rate 54.24% 40.13% 83.79% 11.90% 52.05%

(Table created by author from data in ACAA Survey Results Form, 2000-2015)

Figure 4. Total CCR Production Amount and Recycle Rate

(Figure created by author from data in ACAA Survey Results Form, 2000-2015)

Figure 5. Coal Fly Ash Production and Recycle Rate (Figure created by author from data in ACAA Survey

Results Form, 2000-2015)

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Figure 6. Bottom Ash Production and Recycle Rate (Figure created by author from data in ACAA Survey

Results Form, 2000-2015)

Figure 7. Boiler Slag Production and Recycle Rate (Figure created by author from data in ACAA Survey

Results Form, 2000-2015)

Figure 8. FGD Production and Recycle Rate(Figure created by author from data in ACAA Survey Results Form, 2000-2015)

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2.4 RADIOACTIVE CONTAMINANTS IN COAL ASH

Typical coal ash contaminants include magnesium, sulfur, chromium, zinc, arsenic, cadmium,

and selenium. A recent environmental study led by Duke University revealed traces of

radioactive elements in CCR, including radium isotopes and lead-210, calling attention to

possible health threats posed by radioactive coal ash exposure.

The source of radium isotopes and lead-210 is coal burning. They are the by-products of

burning uranium and thorium content in coal. Vengosh and his team found that radium isotopes

and lead-210 are produced mainly when passing through the boiler and precipitator, and that they

are concentrated in bottom ash and fly ash (Lauer et al., 2015). Radioactivity levels in fly ash are

found to be up to five times greater than in soil and ten times greater than in coal. Lead-210 is a

small element that is likely to attach itself to fine particles in fly ash, thus it easily becomes

airborne after disposal into landfills. By comparing samples of parent coal and coal ash,

researchers found that the ratio of radium to uranium in parent coal is consistent with the ratio in

CCR. The average level of radioactive elements found in this research is listed in Table 3.

Table 3. Radioactivity Concentration in CCR and Coal

Sample Site Element Average APP CCR (Bq/kg) Average APP Coal (Bq/kg)

Appalachian

238U 171 19.5226Ra 170 22.9210Pb 193 21.3228Ra 113 13.8

Illinois

238U 228 30.3226Ra 230 30.7210Pb 286 26.8228Ra 67.5 8.20

Powder River

238U 114 12.0226Ra 120 14.4210Pb 131 11.9228Ra 93.3 13.7

(Table created by author from data in Lauer et al., 2015)

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There is no regulation of radioactivity in CCR, and it is hard to estimate the amount of

released radioactive contaminants and their effect on human health. While the effects of nuclear

and medical radiation exposure effects on humans are studied extensively, the effects of coal ash

radiation exposure remain unknown.

2.5 HAZARD

The hazard related to coal ash depends on the type and amount of heavy metals in the parent

coal. These metal elements are soluble and can easily leach into the aquatic system. In research

on a coal ash spill in Tennessee (Ruhl et al., 2009), they found calcium, magnesium, aluminum,

strontium, arsenic, barium, nickel, lithium, vanadium, copper, and chromium in the water and

soil samples collected, as well as radionuclides. This research compared local Kingston soil and

water with those near the spill and analyzed both upstream and downstream bodies of water.

Other studies have also discovered traces of radioactive elements in coal ash (Silva et al., 2012).

Coal ash can cause respiratory disease (Silva et al., 2012), congenital disabilities (Zierold

et al., 2015), cardiovascular disease (Ladenson, 1990; Ruhl et al., 2009), and nerve damage

(Zierold et al., 2016). These diseases are mostly related to skin, lung, and bladder cancers. Heavy

metal exposure can additionally result in liver, leukemia, breast, and bone cancers. There have

been discussions about exposure to coal ash increasing cancer risk around a major coal ash

landfill in Pennsylvania. Many residents describe having a hard time breathing and a serious loss

of strength. They believe the change in their health is because of coal ash dumping not far from

their homes. As fly dust, coal ash can also increase the amount of pollutants in the atmosphere: it

can be transported by wind to population centers even though the landfills are in rural areas.

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Further, the ash that can be carried far away by wind is usually made up of fine particles (PM10

and below), which are more likely to penetrate deeply into lung tissue and cause respiratory

conditions. Thus, the health of people far from landfills is also at risk. The EPA issued the Clean

Air Act to regulate CCR transportation and dumping. It estimates that this act will save 230,000

lives per year by 2020.

Children’s health can be significantly affected by exposure to coal ash: effects can

include respiratory disease and death. These effects are hard to study because some of them do

not appear until adulthood. Because air pollution is part of the environmental effect of coal ash,

there are studies that try to link air pollution and infant death. One study done by Glinianaia et al.

(2004) focused on particulate air pollution and made significant efforts to avoid confounding

factors such as geographic areas, but there were no apparent correlations found. They explained

the negative statistical results through data inconsistency and missing data. Glinianaia et al.

(2004) was not the only study that failed to relate air particles to infant mortality.

Considering that health effects may not appear until later in life, some research sought to

prolong the study period to 20 years to cover children into their early adult lives. But such

epidemiology studies are usually affected by many confounding factors. Some suggest

conducting biology and toxicology studies in a laboratory setting. However, chronic effects are

hard to mimic in a lab environment, and lab studies are not cost-effective. There are other

toxicology and biology studies that have discovered a negative correlation between coal ash

exposure and health effects. One of these studies was conducted by Pracheil et al. (2016) on

multimetric fish health response after a coal ash spill at the Tennessee Valley Authority’s

Kingston Fossil Plant. In the study, researchers collected more than 1,000 fish samples from five

sites, two of which were reference sites, and measured 20 health metrics. Their results suggested

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that coal ash exposure through water has minor effects and that coal ash ingested in this way is

likely to be eliminated from the system after three years. Another study done by Finger et al.

(2016) discovered that chronic ingestion of coal ash had a minor health effect on juvenile

American alligators. They investigated alligators with contaminated diets for 25 months, and the

difference between the control and test group was statistically insignificant.

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3.0 THYROID DISORDERS

The existence of radioactive contaminants in coal ash is supported by several studies (Głowiak et

al., 1980; Lauer et al., 2015). Głowiak (Głowiak et al., 1980) measured exposure dose that could

quantitatively describe the health hazards of coal ash through the accumulation of radioactive

elements in human organisms. They estimated that 15 deaths could be related to radioactive

pollutants from coal ash emission every 10,000 people near a coal-fired power plant. The amount

of radioactive contaminants in the thyroid are found to be high. The primary distribution of

radioactive contaminants intake in the thyroid was inhalation and ingestion. It is important to

know that the accumulated health hazards of coal ash continue to increase with time.

3.1 BIOLOGICAL PROFILE

The thyroid is a gland located on the lower front side of one’s neck, just below the larynx. In its

normal condition, the thyroid, weighing only 15 to 25 grams, can barely be felt through the skin.

However, it becomes more apparent when it enlarges. Hormones from the thyroid are of two

types: triiodothyronine (T3) and thyroxine (T4). These hormones travel around the human body

through the bloodstream. An important gland affecting thyroid behavior is the pituitary gland.

The pituitary gland is at the lower posterior of the brain, regulating thyroid activities by

generating thyroid-stimulating hormone (TSH).

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Thyroid hormones affect all kinds of cells and play an important role in balancing cell

production and metabolism. They increase energy use and metabolic rate, which results in higher

protein production, glycometabolism, and fat tissue utilization. Thyroid hormones stimulate the

synthesis of estrogen, which affects female reproductive system development. Thyroid disorders

in the female population are an important health topic because of their influence on the

reproductive system, body growth, and the aging process. Dysfunction of the thyroid can also

have adverse health effects that involve the digestive system, the nervous system, and the

circulatory system.

3.1.1 Thyroid disorders

About 12 in every 100 people experience a thyroid disorder during their lifetime. The American

Thyroid Association estimates that about 20 million Americans suffer from thyroid disorders and

that 12 million of those people are unaware of their condition. There are seven common thyroid

disorders: hypothyroidism, hyperthyroidism, goiter, Graves’ Disease, Hashimoto’s Disease;

thyroid nodules and thyroid cancer (McNamara, 1993). In most cases, hyperthyroidism and

hypothyroidism do not co-occur. But there are some exceptions in Hashimoto’s Disease, which

makes its diagnosis more difficult than others. Some thyroid diseases cause only mild symptoms,

making the condition hard to identify. Most conditions require regular monitoring for life. The

most common cause of thyroid disorders worldwide is the inappropriate amount of iodine intake.

3.1.2 Hyperthyroidism

When hypersecretion of thyroid hormones occurs, metabolism is increased, resulting in

accelerated proteolysis. Patients with an overactive thyroid may experience increased heart rate,

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extreme nervousness, weakness, increased appetite, diarrhea, sweating, dramatic weight loss, and

skin ailments (Burrow et al., 1989; Diven et al., 1989; Mullin et al., 1986; Visscher, 1980). It is

common to associate cardiovascular disorders with hyperthyroidism. For example, atrial

tachyarrhythmias are found among 10-22% of hyperthyroid patients. Mitral valve dysfunction is

a problem that arises specifically in women with Graves’ disease. Finally, heart failure is a major

concern, although its relationship to hyperthyroidism is controversial and not completely

understood (Ladenson, 1990). Hyperthyroidism can lead to congestive heart failure and the need

to limit exercise (Klein, 2001). If uncontrolled, hyperthyroidism often leads to the heart

conditions mentioned above and, ultimately, this can result in coma and death (Gott, 1992).

3.1.3 Hypothyroidism

When production of thyroid hormones is low, it leads to a condition known as hypothyroidism. It

is often the consequence of autoimmune destruction of the thyroid gland. It may also result from

surgery or radioactive iodine treatment for hyperthyroidism. The resulting decrease in the thyroid

hormones leads to apathy, depression, listlessness, a slow pulse rate, weakness, coarse hair,

constipation, and skin complications (Burrow et al., 1989; Hamburger 1970; Mullin et al., 1986).

Clinically significant cardiovascular complications occur, including pericardial effusion, which

was present in no less than 30% of untreated patients (Ladenson, 1990).

Additionally, a complicated relationship exists between ischemic heart disease and

hypothyroidism. Bastenie and colleagues (1971) argued that hypothyroidism could potentially

cause coronary heart disease. A review of previously reported studies (Klein, 2001) reveals some

inconsistency in the prevalence of hypertension among hypothyroidism patients. Some suggest a

frequent occurrence, whereas others find no association between them: for the time being,

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evidence is inconclusive concerning the relationship between hypertension and hypothyroidism

(Bergus et al., 1999; Fletcher & Weetman, 1998).

3.1.4 Hashimoto’s Thyroiditis

Hashimoto’s thyroiditis, or Hashimoto’s disease, is an autoimmune disease that is also called

lymphocytic thyroiditis. Hashimoto’s disease was the first identified human autoimmune disease,

found by Japanese specialist Hakaru Hashimoto in 1912. It is not communicable, and its

mechanism is still not clear. It is possibly the result of both genetic and autoimmune factors,

according to recent medical theory (Burek et al., 2009). About 90% of Hashimoto’s thyroiditis

occurs among middle-aged females. Those with a family history of thyroid disorder have a high

risk of Hashimoto’s thyroiditis. Affected females can have irregular menstruation and pregnancy

difficulties. Hashimoto’s thyroiditis has a long disease course, with several possible

complications as one’s immune system is progressively damaged. Less than 5% of patients will

develop hyperthyroidism, but most patients have hypothyroidism in the late stage of

Hashimoto’s thyroiditis (Haugen et al., 2016).

Healthcare providers often take medical history and epidemiological study discoveries

into account, paying more attention to patients in high-risk age groups and those who have a

family history of thyroid dysfunction. Most Hashimoto’s patients will require medical care

throughout their lives, needing medication for not only the disease itself, but also for its

complications (Haugen et al., 2016).

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3.1.5 Graves’ disease

Graves’ disease is an autoimmune disorder that causes the thyroid gland to become overactive,

resulting in hyperthyroidism. Symptoms include restlessness, fast heartbeat, decreased body

weight, being easily irritated, and bulging eyes. Some research suggests that both environmental

and genetic factors influence the occurrence of Graves’ disease, but the exact mechanism

remains unknown. A few epidemiological case-controlled studies indicate Graves’ disease

patients usually have more stressful lives, or have experienced more stressful events 12 months

before diagnosis, compared to control groups (Matos‐Santos et al., 2003; Winsa et al., 1991;

Tomer & Huber, 2009).

3.1.6 Thyroid nodules

Thyroid nodules are defined as the abnormal growth of thyroid cells that form a lump in the

thyroid gland. The lesion tissue is different from surrounding parenchyma and can be examined

by medical tests. Nodules are most commonly seen in areas where the population suffers from

severe iodine deficiency. Many pregnant females and elderly patients have this problem. Thyroid

nodules can be the result of several disorders in the human body. In addition to iodine deficiency,

other major causes include thyroid overgrowth, thyroid cysts, chronic inflammation of the

thyroid, and multinodular goiter. The patient could have a single or multiple nodules, with the

latter being more common. Thyroid nodules range in size from millimeters to centimeters and

can be difficult to detect. Size is not an indicator of malignancy, but approximately 8-16% of

nodules are malignant (Solomon et al., 2015).

According to a systematic review in 2016 (Wiltshire et al., 2016), approximately 63,000

new thyroid cancers occur in the US each year. The incidence has been rising for the last three

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decades. This could be the result of an increase in the use of radiological procedures for the

diagnosis of thyroid nodules. Recent estimates from the American Cancer Society (ACS)

identify about 56,870 new thyroid cancer cases and about 2,010 deaths from thyroid cancer in

the US in 2017. The incidence rate increased more rapidly among females than males in the past

13 years (Figure 9). Deaths for both sexes rose gradually over the same period (Figure 10). The

same trends have been found in other research results (Shi et al., 2017; Sipos & Mazzaferri,

2010; Davies & Welch, 2014).

Figure 9. Estimates of Thyroid Cancer New Cases (2005-2017)

(Figure created by author from data in ACS Cancer Facts and Figures)

Figure 10. Estimates of Thyroid Cancer Deaths (2005-2017)

(Figure created by author from data in ACS Cancer Facts and Figures)

3.2 ENVIRONMENTAL RISK FACTORS FOR AUTOIMMUNE THYROID DISEASE (AITD)

Strong evidence has been provided by epidemiological studies (Tomer et al., 2009) that bacterial

and viral infections are important environmental exposure sources for AITD. The pathogens

involved include Yersinia enterocolitica, Borrelia burgdorferi, retroviruses, Coxsackievirus,

Hepatitis C virus (HCV), and Helicobacter pylori. Epidemiological studies have discovered a

seasonal and geographic difference in the occurrence of AITD (Tomer et al., 2009), which is also

xxvii

associated with pathogen activities and distribution, indicating that infection could be an

environmental trigger for AITD. For instance, Yersinia antibodies have been reported to be

found in over 75% of Graves’ disease patients. Retroviruses have also been found to be closely

associated with Graves’ disease. Studies on HCV infection and thyroid autoimmunity suggest a

greater risk of AITD among HCV patients.

While a specific amount of iodine intake is essential for the thyroid gland to function

normally, excessive consumption can result in autoimmune thyroid dysfunction. In a five-year

cohort study in China, researchers found that prevalence of autoimmune thyroiditis was

significantly different among groups with variable iodine intake (Teng et al., 2006). However, no

significant difference was found between the group with more than adequate iodine intake and

the group with excessive iodine intake. The prevalence of Hashimoto’s disease also differed

significantly. Another study (Fei et al., 2016) has also demonstrated an increase of autoimmune

thyroiditis incidence in regions of high iodine consumption. However, this effect may be

temporary. In one study in 2003 (Dittmar & Kahaly, 2003), thyroid antibody levels decreased

after iodine intake was reduced, and some patients’ antibody levels returned to the normal range.

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4.0 CROSS-DISCIPLINE STUDIES AND DISCUSSION

No previous research directly relates coal ash with thyroid disorders. Some epidemiology studies

have discussed the possible correlation between thyroid problems and coal mining, and some

environmental studies focus on whether chemical compounds in coal could trigger thyroid

disorders. Epidemiology studies on coal ash-thyroid effect is rare. One possible reason is that

thyroid health effects require a long time to develop and are hard to connect with coal ash on a

clinical level. The current short-term epidemiological research is inadequate to cover thyroid

disorders. Biological reactions and dose response, which are commonly used in toxicological

studies, might not have positive results, either. Thus, research principles often used to estimate

correlations are unlikely to prove the possibility in this case. Even with current technology, it is

hard to mimic the long disease course and complicated procedures that could potentially account

for thyroid disorders.

Although the adverse health effect of coal ash on humans is strongly supported by

biology and epidemiology evidence, evidence on thyroid disorders remains inconclusive. In

research done by Gaitan et al. (1993), the health effects of coal water in iodine-sufficient areas

with a high goiter prevalence were discussed. The research focused on the organic compounds in

water that leaked from nearby coal shale. Controlled in vivo and in vitro experiments were

performed on rats. In human goiter conditions, symptoms include body weight loss and

enlargement of thyroid gland. The same symptoms were monitored in the research done by

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Gaitan et al. (1993). Long-term results from the in vivo experiment results showed no significant

difference in body weight between the control group and test group. But differences existed in

the size and structure of subjects’ thyroids, as well as the hormones their thyroids released. Thus,

the researchers concluded that epidemiology observation of goiters caused by coal-water

drinking in an iodine-sufficient area is now supported with scientific experiment evidence. And

drinking coal-water is high risk behavior, because the contamination of water by organic

materials in coal rocks posed a severe risk of thyroid disorders for people in the area. In other

research, Dogra et al. (1995) discovered that being exposed to Cd, one of the toxic metals in coal

fly ash, could damage immunization function in rats. This result was supported by other research

that demonstrated that there was a suppression effect on lung immunization when inhaling Cd

(Blum et al., 2014).

Populations living in areas close to landfills get the most direct coal ash exposure through

water, soil, and air, but those who live away from landfills are also at risk. Fine particles in coal

ash are likely to be transported to other areas, including densely populated cities. It is reasonable

to correlate respiratory disease (which has visible symptoms and is relatively easy to diagnose) to

coal ash exposure in large population centers. On the other hand, causes of thyroid disorders are

more complicated and harder to connect with environmental contributors. If there is a correlation

between them, it would most likely be indirect because coal ash predominantly affects human

health through inhalation and consumption. Many researchers believe it is unlikely that thyroid

problems are directly associated with coal ash exposure. However, it is possible that this lack of

correlation is the result of a dearth of research on this topic.

As mentioned above, many thyroid disorders occur because of malfunctions in the human

autoimmune system. One possible way for coal ash exposure to cause thyroid disorders is for

xxx

coal ash to cause dysfunction in the immune system, with thyroid problems occurring as the

result of immune system disorders. Much research has provided evidence that heavy metal and

radionuclide exposure have severe health impacts on humans. Metal toxins are stored in soft

tissue and radionuclides will gradually enter the blood and circulate throughout the body. Both

metal toxins and radionuclides remain in the human body for a lifetime: it is highly possible that

they could cause immunological and neurological disorders. Some particular heavy metals, such

as cobalt, can directly cause thyroid goiters (Cao et al., 2010).

The model of how environmental exposure could result in autoimmune thyroid condition

onset is well studied in research done by Tomer and Huber in 2009. The model says that the

occurrence of AITD has two main contributors: a genetic predisposition and environmental

exposure. The genetic predisposition means that there is a gene sequence that significantly

increases the susceptibility to AITD in certain external environments. This definition is also

widely used in FNA technology improvement. In AITD, genes involved include TSH receptor,

human leukocyte antigen-DR3, cytotoxic T lymphocyte-associated factor, CD40, and

thyroglobulin. Environmental exposure acts as a trigger in this model, initiating AITD and

possibly maintaining the condition through prolonged chronic exposure. Hansen et al. (2006)

estimated that about 79% of the susceptibility to AITD has a genetic basis. The rest is

contributed by environmental exposure. Environmental triggers include iodine consumption,

medication, smoking, stress, environmental toxicants, and radiation. When focusing on one of

these triggers as the main environmental exposure source, we can treat the others as potential

confounding factors to reduce their influence on thyroid disease outcome.

For future research on this subject, chronic coal ash exposure should be studied as an

environmental trigger for AITD.

xxxi

Radiation exposure is highly possible to be an environmental trigger to thyroid disorders.

As Brent et al. (2010) stated, “Radiation is perhaps the best characterized environmental

exposure linked to effects on the thyroid.” Previous studies on environmental radiation exposure

focused on two sources: medical radiation and nuclear bomb or accident radiation. In treatment

for Hodgkin’s disease, 131I is usually used in external radiation. Graves’ disease along with

hypothyroidism and hyperthyroidism were found among patients who went through radiation

treatment. In TSH receptor tests, low thyroid autoantibody level can be correlated with Graves’

disease manifestation after medical radiation exposure. In nuclear incident radiation exposure

cases, the results are not as consistent as in medical radiation cases. The inconsistency occurs

between initial follow-up studies after nuclear incidences and later long-term follow-up studies.

In most initial follow-up studies, researchers observe an increase of AITD among populations

that experienced radiation exposure.

This result is supported by studies in both Japan and Chernobyl. In the cohort study done

by Nagataki et al. (1994), 2,856 subjects were recruited. They used health examination records

including ultrasonic scanning to make a proper diagnosis and observed a concave dose-response

relationship between AITD and nuclear radiation exposure. The researchers took possible

confounding factors into consideration such as age, sex, and other radiation exposure. However,

more recent studies do not show the same conclusion. In 2006, Imaizumi et al. conducted

research to evaluate thyroid disorders among nuclear bomb survivors in Hiroshima and

Nagasaki. While there was a significantly high prevalence of thyroid nodules, no conclusive dose

response was observed in AITD.

Regarding this inconsistency, it is possible that AITD happens in a certain time window

not long after radiation exposure and that thyroid conditions can be improved in later life either

xxxii

naturally or with medical treatment. Another possible explanation is the survivor bias in the

long-term follow-up study. Survivors who participated in the follow-up study may have longer

life expectancy than the original population that was exposed to radiation materials. This

survivor bias is different from participants’ motivation bias. Participation bias could result in a

higher disease prevalence. The exact influence depends on the participation rate among the target

population. Survivor bias, on the contrary, may cause a lower disease prevalence or even a

negative correlation. Survivor bias might not present in chronic coal ash exposure studies

because the radiation amount is usually small and the death rate is low.

As mentioned previously in this paper, traces of radioactive elements are also found in

coal ash, and it is possible for them to be transported in wind flow among fine ash particles. Both

residents near coal ash landfills and city populations are at risk of suffering radiation exposure

from coal fly ash. Thus, like medical and nuclear radiation, coal ash radiation could be a

potential environmental trigger for autoimmune thyroid disorders among people with genetic

predisposition.

xxxiii

5.0 CONCLUSION

Using a method of literature review, this paper explored the relationship between coal ash and

thyroid disorders. In the absence of positive link in previous studies, this paper put the focus on

the possible health effects of radioactive elements in coal ash.

Coal ash is the by-product of coal burning. As coal remains the predominant source of

electricity, coal ash is mainly produced through power plants. Most coal power plants are located

in Kentucky, West Virginia, Pennsylvania, and Indiana. The coal ash storage landfills are also

located within or around these states. Coal ash poses a significant risk for population life around

power plants and landfills. It can cause respiratory disease, congenital disabilities, cardiovascular

and neurological disease, and cancer. Children and pregnant women are at a greater risk. As

stated before, thyroid disorders are common diseases among the US population. Twelve percent

of the population experiences some degree of thyroid dysfunction during their lifetime. Besides

hormone disorders, thyroid dysfunction has several complications that affect human lives, such

as heart failure, exercise limitations, and diarrhea. More severe effects include cancer, coma, or

death.

In this paper, previous research about coal ash and thyroid disorders are briefly

introduced. This includes the production, disposal and recycling of coal ash, radioactive element

traces and health risks, as well as common thyroid disorders and environmental risk factors for

AITD. The discussion provided evidence supporting radioactive exposure affecting thyroid

xxxiv

behavior. In addition, a possible connection between coal ash exposure and thyroid disorders is

drawn based on the discovery of radioactive elements in coal ash.

This paper has several limitations. First, no new research was conducted for this paper.

Discussions and assumptions about coal ash exposure and thyroid disorders were based on a

literature review of previous studies. Without new quantitative data, the discussion of possible

correlation is less convincing. Another limitation was due to a lack of information. References in

this paper were only in English, and some of them were studies dating back 30 years. Only 47%

of the references were from the past decade. The third limitation was that some of the references

were epidemiology or exposure studies instead of laboratory experiments. In these epidemiology

and exposure studies, there might have been important confounder factors that were not taken

into account. The combination of such, can affect the conclusion in this paper.

This all has implications for future research. First, more studies need to be done on

radioactive contaminants in coal ash. Although similar elements were also found in the exposed

area of nuclear accidents, their effects might be different. Radioactive contaminants in nuclear

bombs are released once, while coal ash radioactive contaminants are released rather regularly

over the year. The radioactive decay in these two types of exposure could be different. Second,

as mentioned before, coal ash radiation could be a potential environmental trigger for AITD

among populations with a genetic predisposition. To further prove or disapprove this correlation,

an exposure research should be initiated.

It should be noted that genetic predispositions that need to be considered include

leukocyte antigen-DR3, cd 40, cytotoxic T lymphocyte-associated factor 4, protein tyrosine

phosphatase-22 gene, thyroglobulin (Tg), and TSH receptor. These genes are usually inherited. A

genetic predisposition puts an individual at a higher risk of developing a certain disease more so

xxxv

than other members of the population. Possible confounding factors include gender, race, age,

pregnancy, iodine intake, family thyroid history, geospatial difference, smoking, other major

sources of radiation exposure, awareness of their thyroid condition, and exposure to toxic

environmental agents (PCBs, organochlorine pesticides, PBDEs, BPA, perchlorate, thiocyanate

triclosan, and isoflavones). There is a possibility that coal ash exposure is also time-related,

meaning that a population new to coal ash exposure is at greater risk of developing autoimmune

thyroid disease. This is an important aspect we need to consider when interpreting study results.

Compared to radiation exposure from nuclear incidents or medical treatment, radiation

from coal ash exposure is much more difficult to observe, measure, and estimate. When

determining proper recruitment radius, we can conduct a six-month pre-research analysis of air,

water, and soil samples to get a stable estimate of coal ash exposure in an area. Even with the

pre-research result, other environmental factors such as wind and rainfall can still produce bias in

the study, and this effect is hard to balance by confounder adjustment. In addition, multiple

environmental toxicants can have complicated health effects that might not be able to be adjusted

among participants through statistical methods.

Despite such difficulties, it is crucial to further study coal ash radiation as an

environmental trigger for AITD. Coal is the primary source of electric power in the US; hence, a

significant amount of coal ash has been produced over the year. The accumulative health effects

of coal ash are increasing by the minute, which cannot continue to be overlooked. Conducting

further research is of significant benefits to public health.

xxxvi

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