COAL WORKERS’ PNEUMOCONIOSIS IN U.S. COAL MINES: A REVIEW OF EXPOSURES, INTERVENTIONS, AND OUTCOMES

by

Timothy William Beck

B.S., Mining Engineering, University of Missouri-Rolla, 2000

Submitted to the Graduate Faculty of

Graduate School of Public Health in partial fulfillment

of the requirements for the degree of

Master of Public Health

University of Pittsburgh

2014

UNIVERSITY OF PITTSBURGH

GRADUATE SCHOOL OF PUBLIC HEALTH

This essay is submitted

by

Timothy William Beck

on

April 4, 2014

and approved by

Essay Advisor:James Peterson, PhD ______________________________________Associate ProfessorEnvironmental and Occupational HealthGraduate School of Public HealthUniversity of Pittsburgh

Essay Reader:Anthony Iannacchione, PhD ______________________________________Associate ProfessorMining EngineeringSwanson School of EngineeringUniversity of Pittsburgh

Copyright © by Timothy W. Beck

2014

ABSTRACT

Despite nearly forty-five years of protective dust rules, U.S. coal miners still experience an

alarming level of coal workers’ pneumoconiosis, a debilitating and deadly lung disease. For

miners that have worked entirely under these dust rules, the probability of developing the second

level of disease or greater should be zero for a 35 year career. Recent surveillance has pegged the

number at over two percent, with eight percent of experienced miners exhibiting some evidence

of the disease. Nearly 1,000 miners and former miners succumb to the disease annually,

establishing it as a serious public health issue, and making it the deadliest mining-related hazard

in the U.S., far ahead of widely publicized roof falls, fires, and explosions.

The National Institute for Occupational Safety and Health and other research

organizations have suggested a series of possible causes for the continued prevalence of coal

workers’ pneumoconiosis, including extended shift lengths, increased mining of higher quartz-

bearing coal and rock seams, and insufficient dust rule enforcement. This paper presents many of

the broader risks for developing coal workers’ pneumoconiosis as well as a discussion of the

impact of specific exposure characteristics.

In the coal dust regulations developed in 1969, a seemingly comprehensive approach to

control exposures was employed: regulation and enforcement, dust control research, medical

surveillance, and worker compensation. While the present system addresses several of the risk

James Peterson, PhD

COAL WORKERS’ PNEUMOCONIOSIS IN U.S. COAL MINES: A REVIEW OF EXPOSURES, INTERVENTIONS, AND OUTCOMES

Timothy W. Beck, MPH

University of Pittsburgh, 2014

factors leading to coal workers’ pneumoconiosis, it fails to account for the disparity between

current documented dust exposures and expected rates of the disease, especially in localized

regions. This paper briefly discusses the activities of each component, noting the successes and

shortcomings experienced. The current approach to worker exposure control is reviewed along

with the prospects of reducing the prevalence of this deadly and debilitating disease.

Recommendations are presented to suggest improved approaches to control exposure to coal

mine dust and prevent the resulting diseases.

TABLE OF CONTENTS

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

1.1 EXPOSURE TO AIRBORNE PARTICULATE MATTER............................3

1.2 U.S. COAL MINING OVERVIEW....................................................................4

1.3 COAL MINE PARTICULATE EXPOSURES..................................................4

1.4 COAL WORKERS’ PNEUMOCONIOSIS.......................................................5

2.0 FACTORS ASSOCIATED WITH CWP..................................................................10

2.1 ENVIRONMENTAL FACTORS......................................................................10

2.2 INDIVIDUAL RISK FACTORS.......................................................................17

3.0 REDUCING CWP IN U.S. COAL MINES..............................................................23

3.1 PRIMARY PREVENTION OF CWP..............................................................23

3.2 SECONDARY PREVENTION OF CWP........................................................30

3.3 TERTIARY PREVENTION OF CWP............................................................32

4.0 RECOMMENDATIONS............................................................................................37

4.1 IMPROVED DUST MONITORING AND CONTROL.................................37

4.2 TARGETED INTERVENTIONS.....................................................................38

4.3 MINER ENGAGEMENT AND PARTICIPATION.......................................40

4.4 INSTITUTIONAL REFORM...........................................................................41

5.0 CONCLUSIONS.........................................................................................................42

APPENDIX A: DEVELOPMENT OF THE TERMINOLOGY OF COAL WORKERS’

OCCUPATIONAL LUNG DISEASES......................................................................................45

APPENDIX B: BRIEF HISTORY OF U.S. MINING HEALTH AND SAFETY

REGULATION TO 1969............................................................................................................47

BIBLIOGRAPHY........................................................................................................................50

LIST OF TABLES

Table 1. Occupational exposure limits for respirable coal mine dusts worldwide (adapted from

[77])...............................................................................................................................................25

Table 2. Respirable coal dust regulatory and recommended exposure limits (adapted from [80])

.......................................................................................................................................................26

LIST OF FIGURES

Figure 1. Wood-cut diagram from Agricola’s De Re Metallica depicting a miner exposed to

“fetid vapors” [3].............................................................................................................................2

Figure 2. CWP morbidity in U.S. underground coal miners by tenure, 1970-2012 [25]................8

Figure 3. Percentage of evaluated miners with rapidly progressive coal workers’ pneumoconiosis

by county [30]..................................................................................................................................9

Figure 4. Probability of a miner being classified as 2/1+ after a 35 year career of exposure to

various coal dust concentrations [31]............................................................................................11

Figure 5. Prevalence of CWP (ILO 1/0+) among U.S. coal miners by estimated exposure [43]..18

Figure 6. Hours worked annually by U.S. underground coal miners, 1978-2007 [17].................19

Figure 7. Operator and inspector coal mine dust measurements, 1979-2003 [14]........................28

Figure 8. NIOSH CWXSP mobile examination unit.....................................................................31

Figure 9. Fatalities at U.S. coal mines, 1900-1969 [17]................................................................48

1.0 INTRODUCTION

Mining in all its forms provides a range of materials that contribute to the wellbeing of society

and advancements in a range of fields. From the familiar metals and stones that build the world

around us to the fuels that power our modern technologies, mining plays an important role in the

world’s prosperity and quality of living. Mining has long been recognized as a distinctly

dangerous occupation. It appears that nearly all historical records of mining afford at least some

mention of the dangers faced by miners. Hippocrates supplied one of the first known

acknowledgements of the hazards in circa 400 BC, when he observed the toxic effects of lead

exposure in miners [1]. Nearly 400 years later, Strabo encountered and described the effects of

sickening mine air in his 7 BC work, Geographica [2]:

“the air in the mines is both deadly and hard to endure on account of the grievous

odor of the ore, so that the workmen are doomed to a quick death. What is more,

the mine is often left idle because of the unprofitableness of it, since the workmen

are not only more than two hundred in number, but are continually spent by

disease and death.”

Though it was widely known that foul air in mines could cause sickness and death, a connection

between the mine environment contaminated with dust and the detrimental effects on the lungs is

described in Georgius Agricola’s 1556 mining treatise De Re Metallica [3]:

1

“the dust which is stirred and beaten up by digging penetrates into the windpipe

and lungs, and produces difficulty in breathing, and the disease which the Greeks

call asthma. If the dust has corrosive qualities, it eats away the lungs and implants

consumption in the body… Women are found who have married seven husbands,

all of whom have this terrible consumption has carried off to a premature death.”

This toxic air is even depicted in the original engraved plates that demonstrate primitive mining

methods, using fire to break rocks and develop tunnels (Figure 1). While Agricola may have

attributed other mining hazards to supernatural subterranean gnomes, he no less recognized that

miners frequently suffered respiratory disease due to their labors underground.

Figure 1. Wood-cut diagram from Agricola’s De Re Metallica depicting a miner exposed to “fetid vapors”

[3].

2

1.1 EXPOSURE TO AIRBORNE PARTICULATE MATTER

Over the past many years, a growing body of evidence has demonstrated associations between

the inhalation of particulate matter and an extensive list of negative health effects. The exposure

to such aerosols, in both workplace and ambient environments, is expressed as a mass per unit

volume of air, or mass concentration (or simply “concentration”). Studies have shown that

increases in the concentration of inhalable particulate matter results in increased deaths from

respiratory illnesses, increased cardiovascular deaths, increased rates of lung cancer and

increased risk of premature births and infant mortality [4], [5], [6], [7]. These small particles are

easily inhaled and not effectively filtered by the nose or upper respiratory system [8]. Produced

by many natural and anthropogenic processes, fine particulate may deeply penetrate the lungs,

causing extensive damage.

Until recently, ambient particulate matter was ubiquitous in industrial areas, playing a

main role in the choking “fog” that claimed several lives during notable mid-20 th century

episodes in Meuse Valley, Belgium, Donora, Pennsylvania, and London, England [9]. Efforts

across the U.S. following the passage of the Clean Air Act of 1970 have significantly reduced

these hazardous ambient particulate concentrations. Between 1990 and 2012, national

concentrations of PM10 (particulate matter with a 50% cut-point of aerodynamic diameter less

than 10 microns) have decreased 39 percent to a 24-hour time-weighted average (TWA) of 63.8

µg/m3, as measured by the U.S. Environmental Protection Agency at hundreds of strategically

located sites [10].

3

1.2 U.S. COAL MINING OVERVIEW

Coal is an abundant mineral resource in the U.S. and provides a relatively inexpensive source of

energy for electric power generation. The production of coal has historically provided substantial

employment, with over 800,000 miners working at the nation’s mines in 1923 [11]. Though

current employment in U.S. underground coal mines has declined to 54,426 in 2012 [12], mining

remains the primary industry in the coalfields of several U.S. states, including West Virginia,

Kentucky, and Illinois [13]. This regional concentration localizes the impact of both economic

and health effects resulting from coal mining on a population with few employment alternatives.

1.3 COAL MINE PARTICULATE EXPOSURES

The level of ambient particulate contamination in U.S. coal mines is measured by both coal mine

operators and inspectors for the Mine Safety and Health Administration (MSHA) and is

presented by the National Institute for Occupational Safety and Health (NIOSH) in their annual

Work-Related Lung Disease Surveillance System report [14]. NIOSH reports that the average

coal miner’s 8-hour TWA exposure to respirable dust was 0.458 mg/m3 in 2012. It should be

noted, however, that as recently as 1995, 42 percent of these individual samples exceeded the

MSHA permissible exposure level of 2.0 mg/m3 [15]. With these elevated exposures in coal

mines come many of the associated health impacts, most notably coal workers’ pneumoconiosis.

4

1.4 COAL WORKERS’ PNEUMOCONIOSIS

Following recent mine disasters at the Sago and Upper Big Branch underground coal mines, in

2006 and 2010, respectively, the U.S. coal industry redoubled their safety efforts, setting record

lows for both injury rates and fatalities in 2012 [16]. These recent successes however may

obscure the fact that thousands of miners continue to succumb to preventable occupational lung

diseases. From 1996 to 2007, coal mining accidents claimed the lives of 415 workers, both on

the surface and underground [17]. During the same time period, coal worker’s pneumoconiosis

(CWP) played a role in the death of over 8,000 individuals, being identified as the primary cause

of death in 40 percent of these cases [18]. This tremendous human cost comes with a

considerable financial burden as well—over $39 billion in federal CWP compensation benefits

have been paid to coal miners over the 25 years from 1980 to 2005 [19].

Coal workers’ pneumoconiosis (CWP), also commonly known as “black lung disease,” is

a progressive lung disease resulting from exposure to high levels of respirable dust that can be

disabling and fatal in its most severe form. CWP is defined as the accumulation of coal dust in

the lungs and the resulting reaction of tissue to its presence [20]. Once contracted, there is no

cure for CWP. The goal, therefore, is to limit worker exposure to respirable dust to prevent

development of the disease. The disease may have a very long latency period, extending into

decades, and be asymptomatic with many of the physical effects remaining hidden until detection

and diagnosis through medical examination [19]. This is in contrast to many other mining

hazards, which manifest themselves in immediate and visible ways. The development of the

terminology used to label and describe this occupational respiratory disease is explored in .

5

1.4.1 Detection and diagnosis

Unlike many other respiratory exposures, the effects of exposure to coal mine dust and initial

development of CWP do not typically manifest in sudden shortness of breath or other ailments.

Instead, living miners must rely on chest radiographs (or x-rays) and functional breathing tests to

identify the presence of this lung damage.

There are two types of CWP: simple and complicated. In chest x-rays, simple CWP

appears as small opacities (10 mm and smaller in diameter) in the lungs, while complicated CWP

presents as larger opacities and fibrotic masses. These chest x-rays are classified by International

Labour Organization (ILO) standards based on the following procedures [21]: lung images

demonstrating simple CWP are grouped based on severity as major category 1, 2, or 3, with

those showing no apparent damage classified as 0. The major category determination may list

other categories if the additional category was “seriously considered” during the classification.

For example, an ILO classification of subcategory 1/0 is reported for x-rays classified as

category 1 after having been seriously considered as category 0 as an alternative. NIOSH uses

the subcategory 1/0 as the lowest possible presentation of the disease for their surveillance work.

Simple CWP may result in minimal functional impairment [22]. While categories 2 or 3 may be

associated with reductions of the maximum ventilatory rates and a slightly lower level of oxygen

in the bloodstream, these irregularities are not enough to cause disability.

The names complicated CWP and progressive massive fibrosis (PMF) are used to

describe the singular condition of exhibiting one or more opacities with diameters exceeding 10

mm on radiograph. Images demonstrating PMF are grouped based on severity as category A, B,

or C, with those showing the least damage classified as A. This condition is most likely to

develop in miners already affected by simple CWP, though it has been found in miners with no

6

previous CWP diagnosis. Another characteristic of this condition is that it may continue to

progress without continued dust exposure. Functional impairments associated with PMF include

breathlessness, chronic bronchitis, and occurrence of right-sided heart failure. PMF is also

associated with decreased oxygen-diffusing capacity and increased mortality [23].

1.4.2 Recent increase in CWP prevalence

Today, CWP continues to be a persistent and significant health threat to underground coal mine

workers. Until recently, the prevalence of CWP in U.S. coal mines had been declining. For

underground coal miners with 25 or more years of experience, the prevalence of CWP had

dropped from over 30 percent in 1970 to a low of 4.2 percent in 1999 [24]. This rate has doubled

to nearly eight percent for the same demographic in the most recent NIOSH surveys conducted

in 2012 [25]. Figure 2 shows this recent increase in CWP (as defined by ILO category 1/0 or

greater) as measured by NIOSH’s Coal Workers’ X-ray Surveillance Program (CWXSP) for

those miners with the most tenure underground.

7

Figure 2. CWP morbidity in U.S. underground coal miners by tenure, 1970-2012 [25].

After the Upper Big Branch disaster in 2010, 24 of the 29 deceased miners were examined by the

West Virginia Medical Examiner for evidence of CWP [26]. Evidence of CWP was found in 17

of the 24 victims (or 71 percent), with four others having “anthracosis”, which is a term that may

be used in place of CWP or to describe an earlier, milder form of the disease. This rate compares

very unfavorably to the NIOSH-documented rate of 10.0 percent for the rest of the miners in the

state of West Virginia [27]. Most startling is that one of the victims with CWP was just 25 years

of age and five of the miners with CWP had worked less than 10 years as coal miners.

Recent NIOSH published reports have shown that a recent increase in rapidly progressing

CWP can be localized to the Central Appalachian Region [28], [29], [30]. These areas have been

referred to as black lung or CWP “hot spots” in the associated literature. Figure 3 shows a map

of the locations experiencing rapidly progressing CWP at rates much higher than expected. In

these black lung hot spots, up to 80% of evaluated miners had evidence that their cases of CWP

8

were advancing at alarming rates. It is apparent that despite numerous attempts to reduce the

incidence of CWP in these areas, the disease remains a significant public health issue and may

require new approaches or more stringent controls to protect miners’ health.

Figure 3. Percentage of evaluated miners with rapidly progressive coal workers’ pneumoconiosis by

county [30].

9

2.0 FACTORS ASSOCIATED WITH CWP

For CWP, many exposure characteristics have been studied extensively with connections

established to resulting disease, while some have been hypothesized, but may lack supporting

evidence. For many of these factors, epidemiological evidence provides a strong link or

association and toxicological studies have demonstrated the plausible biological mechanisms

responsible for the development of CWP pathologies. These factors can be grouped into general

properties of the work environment and individual characteristics that may transform the various

environmental exposures into personal negative health effects.

2.1 ENVIRONMENTAL FACTORS

2.1.1 Mass concentration

Much of the CWP literature has focused on the mass concentration of respirable coal dust as a

measure of occupational dust exposure. Early studies of British miners were used by Jacobsen et

al. to produce one of the first quantitative exposure-response relationships for coal dust

exposures by mass concentration [31]. This exposure-response curve, shown in Figure 4,

illustrates that as one is exposed to increasing concentrations of respirable coal mine dust, the

predicted risk of developing CWP increases. This same relationship compares favorably to

10

studies of U.S. coal miners, demonstrating the increasing risk of developing CWP classified as

ILO category 1/0 or greater after working for 45 years in increasingly dusty mine atmospheres

[32]. As further evidence that lower occupational exposures to mass concentrations of respirable

dust may reduce disease burden, studies of former U.S. miners at autopsy have shown that

working under the reduced dust standards from the Federal Coal Mine Health and Safety Act of

1969 (the Coal Act) has reduced both the prevalence and severity of lung damage associated

with CWP. Progressive massive fibrosis (PMF), the most severe stage of CWP, has been

identified in 9.6 percent of miners who worked prior to 1969, while for those who worked post-

1970, 1.2 percent [33]. Although additional exposure characteristics are frequently integrated

into the epidemiological analysis, mass concentration has consistently been associated with the

prevalence and progression of disease [30].

Figure 4. Probability of a miner being classified as 2/1+ after a 35 year career of exposure to various coal

dust concentrations [31].

11

2.1.2 Particle size

Particulate concentrations have been typically measured as a mass-based concentration because

mass is relatively easy to measure with current techniques and health-effects have been shown to

be well-correlated with the mass of respired particles [34]. Many epidemiological studies support

this approach, showing increasing adverse health effects with increasing particulate mass

concentrations [4], [5], [6], [7].

Recent advances in nanotechnology have allowed the measurement of increasingly

smaller particles with corresponding increases in surface area per unit mass. Toxicological

studies have followed, showing that smaller particles can cause stronger adverse biological

reactions, especially inflammation and release of reactive oxygen species (ROS), than the same

mass concentration of larger particles [35]. While several coal mine particle size studies have

been undertaken in response to associations between coal dust exposure and chronic obstructive

pulmonary disease, this research has mainly focused on thoracic particles, larger than those of

respirable size [36], [37]. Currently, there is little published field data on the size distribution of

coal mine dusts in the submicron to micron range. For this reason, the toxicology of small

particles have not been adequately studied in coal miner populations, though this has been

suspected to impact current rates of disease by NIOSH [15].

2.1.3 Coal and coal dust composition

Coal is a complex heterogeneous mixture of more than 50 different possible elements [38]. Many

of these elements are oxidized producing many more potential compounds. Composed primarily

of organic matter, the amount of inorganic compounds can range from nearly zero to 50 percent

12

by weight. These “contaminants” can include phyllosilicates, quartz, carbonates, sulfides,

sulfates, and other minerals [39]. The main metals are iron and aluminum, with arsenic,

cadmium, cobalt, copper, nickel, and zinc representing trace fractions. The composition of coal

varies widely from coal seam to coal seam, and frequently within the same seam [40].

The dust found in underground coal mines has been estimated to be between 40 and 95

percent coal [15]. The remainder consists of dusts from the surrounding strata or from rock

(limestone) dust applied to prevent both the occurrence and the propagation of explosions. While

coal dust composition may not mimic that of bulk coal, studies have suggested that using bulk

coal data can provide a good approximation of the potential makeup of coal mine dust [41].

Many studies have established connections between these components of coal and coal dust and

resulting incidence of CWP, with the most frequently discussed contents being carbon, quartz,

and iron [42].

2.1.3.1 Carbon content

Coal rank is the common term used to differentiate between the carbon content of different coal

deposits. High rank coals are considered to contain 89–90 percent carbon, while medium/low

rank coals contain 80–89 percent carbon [43]. Epidemiological studies have linked a higher risk

of developing PMF over a working lifetime to miners exposed to similar levels of respirable dust

of high rank coal [43]. Another study looking at functional impairments found that miners in the

high-rank coal mines of the Midwestern and eastern U.S. had greater loss of lung function than

miners from the western U.S., where low-rank coals are common [44]. These studies corroborate

the findings of the Mining Research Establishment in Great Britain. Based on exposure to a 2.0

mg/m3 respirable dust concentration of coal with 86.2 percent carbon content, the resulting risk

of developing PMF after a 40-year working career has been calculated at 1.19 percent and 7.75

13

percent for simple CWP [45]. For coals with carbon content of 83 percent, in the middle of the

medium/low rank range, the risks decreased to 0.71 percent for PMF and 6.49 percent for simple

CWP. Because of the influential effect that coal rank has on the occurrence of CWP and PMF,

some groups, including American Conference of Governmental Industrial Hygienists (ACGIH)

have called for exposure limits to be established based on the rank of coal being mined [46].

2.1.3.2 Quartz content

For many years, respirable quartz (also referred to as crystalline silica) dust was considered the

active agent in the development of CWP. While quartz dust “dose and composition do not appear

to account wholly for changes in the prevalence of CWP” [47], the fibrogenic properties of

quartz are well connected to lung pathology and respiratory impairment. Research has shown a

wide variation in the risk of quartz exposure in U.S. coal mines, based on the origin of the quartz

content or its interaction with other chemicals and minerals in the airborne dust. For this reason,

epidemiological studies have produced divergent results with different dose-response curves for

CWP with similar quartz exposures [32]. These relationships have been especially challenged to

predict CWP at low quartz concentrations, though it is expected that coal dust exposures are the

dominant toxic hazard in these situations [48].

As the thicker coal seams in the U.S. are depleted, mines are left with thinner seams to

exploit. In order to mine these thinner seams while maintaining equipment clearance, some

operations will intentionally remove portions of the rock above and below the seam [28]. Pollock

et al. report that in these cases, from 20 to 30 percent of the mined material is pure rock. These

modern coal seams also tend to be less continuous and contain more rock partings. Rock partings

within the coal and areas where the coal is not present typically contain much more quartz than

the coal itself [49]. There is some epidemiological connection between these quartz exposures

14

and CWP, with U.S. research finding a significant relationship between the mining of thinner

seams of coal and rock and the occurrence of CWP [50]. For those miners working in seams less

than sixty inches in height, the risk of being located within a black lung hot spot region is 8.6

times higher than that for miners working seams five feet or taller. These results are consistent

with British research that associated increases in CWP prevalence with cutting of rock [51].

2.1.3.3 Iron content

One of the long-recognized contaminants within coal is iron pyrite, chemical formula FeS2.

While pyrite is frequently connected to the risk of spontaneous combustion in coal mines,

exposure to iron-bearing dusts may be relevant to the development of CWP. Researchers have

noted accumulations of iron in the lung tissue of CWP victims, suggesting that iron’s ability to

catalyze oxidant production may contribute to the onset of pneumoconiosis [52]. A recent

toxicological study demonstrated that coals with the highest pyritic sulfur and available iron

generate the greatest inflammatory stress response, an indicator of lung distress, and a potential

precursor to the development of CWP [53]. This agrees with a post-mortem study that found that

lung iron content correlated well with the degree of CWP [54].

Huang et al. have extensively examined the incidence of CWP and numerous components

in coal, finding a strong positive correlation between both sulfur and bioavailable iron, though

they did not identify a similar effect for coal rank or crystalline silica/quartz [41]. Because the

levels of iron are much higher for eastern coals than for those in the West, this result may be an

artifact of the demonstrated regional concentration of CWP (Section 1.4.2). Because of the

complex nature of coal dust and interactions between compounds, separate effects for the range

of coal constituents can be difficult to establish [48].

15

2.1.4 Mine size and location

While rates of CWP are currently increasing in mines of all size, NIOSH researchers have shown

that both CWP and PMF are much more prevalent among worker from small mines (those with

fewer than 50 employees) [55]. These small mines also have a 10 times greater likelihood of

being in a black lung hot spot region than larger mines with 500 or more employees [50]. A

robust analysis of MSHA citation and noncompliance data from 1999 to 2002 indicates that there

is no clear relationship between an increased number of citations issued and a mine’s likelihood

of being located in a CWP hot spot region [50]. In fact, the research found that fewer than seven

percent of mines in the hot spot regions received citations pertaining to the permissible dust

limits, while twenty percent in other regions received similar citations. By contrast, when

considering violations due to excessive concentrations of quartz dust, the hot spot mines

exhibited a significantly higher proportion of citations than those mines in other areas, indicating

a higher exposure to coal dusts containing hazardous levels of respirable quartz dust. This

analysis suggests that small mines may not have the resources to effectively provide protection

for workers, including integration of state-of-the-art approaches to dust suppression and

acquisition of personal protective equipment, such as respirators.

16

2.2 INDIVIDUAL RISK FACTORS

2.2.1 Age and total lifetime dust burden

Age has been shown to be a risk factor for the development of CWP [45]. This likely stems from

the increased cumulative dust exposure for older individuals compared to younger workers.

Chronic dust exposures, even at levels below the current 2.0 mg/m3 standard, can produce

substantial accumulation in the macrophages of the lung. Because lung clearance rates are

reduced by lung burden [56], high exposure intensities, even for just five years, can result in

clearance times that extend for another 25 years [57]. This extended residence time of inhaled

particles in the lungs provides an increased opportunity for immunological response, such as

chronic inflammation and fibrogenesis.

Cumulative dust exposure has been shown to be a strong predictor of CWP risk [58].

Figure 5 shows this relationship for U.S. coal miners [43]. As indicated in the figure, exposures

over a 45 year career at a concentration of 2.0 mg/m3 result in rates of CWP ranging from 14 to

24 percent, depending on coal rank. Because many of the samples collected for compliance

exceed the 2.0 mg/m3 value, miners are achieving their permissible lifetime accumulation in

fewer years of tenure and accumulating much higher amounts of dust over a working career than

permitted by the law [15].

17

Figure 5. Prevalence of CWP (ILO 1/0+) among U.S. coal miners by estimated exposure [43].

Note: Exposure to 2.0 mg/m3 for 45 years is equivalent to 90 mg--years/m3 as shown.

2.2.2 Shift length and time between work shifts

U.S. coal miners continue to work more hours annually, working both longer and more frequent

shifts [17]. The increase since 1978 in annual time worked can be seen in Figure 6. Case studies

of workers at two British mines have indicated that working extended hours may cause an

increase in CWP prevalence [51]. Although only weak epidemiologic connections have been

established between miners working extended shifts and rates of CWP, miners working 12 hours

are theoretically exposed to 50 percent more dust than workers with 8 hour shifts. As has been

discussed in the previous section, this increase in cumulative dust burden over a career will

increase the risk of developing CWP. Longer shifts also pose the problem of reduced lung

clearance times for workers who work consecutive shifts. This can overwhelm lung clearance

mechanisms and result in significant accumulations of dust particles, reduced breathing capacity,

and development of CWP [56]. Unfortunately information about shift lengths is not miner-

18

specific in the U.S., but rather mine- or industry-specific. This makes it increasingly difficult to

make a formal epidemiologic analysis for workers in U.S. coal mines.

1978 1983 1988 1993 1998 20031500

1600

1700

1800

1900

2000

2100

2200

Year

Hour

s wor

ked/

unde

rgro

und

min

er

Figure 6. Hours worked annually by U.S. underground coal miners, 1978-2007 [17].

2.2.3 Use of respirators and personal protective equipment

Because CWP results from exposure to coal dust, it is largely preventable through the use of

respirators. A common, inexpensive half-face respirator typically provides a protection factor of

10, reducing the wearer's concentration to 10 percent of the workplace concentration [59].

Though this application would greatly reduce the occurrence of CWP, barriers are present which

inhibit respirator use.

On the individual level, coal miners may neglect to use respirators during their activities

because there may be a lack of awareness about the hazards and consequences, a lack of

knowledge on the proper fit and use of respirators, or even a perceived lack of personal control

over their health and wellbeing. Tobacco use may also limit respirator use, with strong inverse

relationships observed between smokers and duration and frequency of respirator use [60]. A

19

recent study of U.S. coal miners has shown that miners may modulate their respirator use to

target dusty tasks, with higher levels of dust exposure being associated with increased respirator

use [61]. An earlier study of U.S. miners found the same effect, with observations and

measurements showing that respirator use is intermittent and that the respirator was not worn

when dust was not visible [62]. This is an important finding, suggesting that information about

the possibly unseen hazards presented by certain activities can increase self-protective behaviors.

For those workers that would wear a respirator, there is the issue at smaller mines of

unavailability of required fit tests and even respirators themselves [63]. Research has also shown

that respirator use is related to establishment size, increasing from 11.5 percent at the smallest

establishments to 56.5 percent at the largest [64]. Because size of mine and respirator use are

closely linked, efforts to improve awareness and access to fit tests, especially among smaller

mines, are needed to reduce the development of CWP.

2.2.4 Smoking status

Although both smoking and dust exposure may be responsible for the development of chronic

obstructive pulmonary disease and loss of lung function, smoking does not appear to increase the

prevalence of CWP or affect an individual’s development of CWP [31]. When U.S. researchers

produced a logistic model of pack-years on CWP and compared it to the same model of age and

dust exposure on CWP, smoking was found to be unable to predict the prevalence of the disease

[43]. This is consistent with earlier British research showing that smoking does not increase the

potency of coal dust [65].

20

2.2.5 Individual immunological factors and health status

Chronic inflammatory diseases, like CWP, are multi-factorial and affected by both

environmental and genetic factors. The underlying immunologic mechanisms and potential

genetic susceptibilities leading to the development of CWP are not clearly understood [66]. Coal

dust has been shown to stimulate an inflammatory and fibrotic response through the release of

cytokines [67]. Investigations into polymorphisms within genes related to these cytokines have

found divergent results in relation to CWP status. A recent study of Turkish miners has

demonstrated a differential distribution in polymorphisms relevant to pro- and anti-inflammatory

cytokines in victims of CWP and control subjects [67]. This finding is in contrast to that of a

similar study by many of the same researchers that no significant difference exists between

control subjects and those with complicated CWP [68].

In addition to cytokines, inflammatory cells secrete reactive oxygen species (ROS) during

the immunological response to dust particles. Imbalances between ROS and antioxidant enzymes

can be used as a marker of oxidative stress. In a study of miners with CWP, levels and activities

of various antioxidant enzymes were elevated, suggesting the presence of oxidative stress due to

free radical formation [69]. This may explain the effects observed for coal miners exposed to

higher levels of bioavailable iron from pyrite (see Section 2.1.3.3) [53].

Other health effects have been shown to be connected to CWP. For example, CWP and

tuberculosis have historically co-existed in the mining workforce. Though CWP does not cause

an increased risk for tuberculosis, the presence of tuberculosis appears to be related to both CWP

incidence and progression [70], [58]. Wiener et al. describe atypical reactions to tuberculosis that

may contribute to the development of PMF from simple CWP [71].

21

Another complication related to CWP is the presence of rheumatoid arthritis (RA), an

autoimmune disease that causes damage through an inflammatory response. In miners with

rheumatoid factor, the autoantibody that contributes to the autoimmune disease process of RA,

rheumatoid pneumoconiosis can develop. This rare condition, also called Caplan syndrome, is

characterized by multiple rounded nodules forming in the lungs over a short period of time, and

may occur in one percent of CWP victims [72]. While there is no evidence that coal mining

predisposes workers to RA, it is unclear whether RA changes the lung’s response to coal dust.

22

3.0 REDUCING CWP IN U.S. COAL MINES

The passage of the Federal Coal Mine Health and Safety Act of 1969 (the Coal Act) established

respirable dust exposure limits, dust sampling requirements for inspectors and mine operators, an

engineering research program to develop and disseminate dust control technologies, a voluntary

chest x-ray surveillance program to identify CWP in underground coal miners, and a benefits

program to provide compensation to affected workers and their families. In an approach first

described by Leavell and Clark in 1965, preventive medicine and associated efforts to prevent

and control disease can be divided into three levels of intervention: primary, secondary, and

tertiary [73]. The approach adopted by the U.S. government to reduce incidence and prevalence

of CWP can likewise be divided into the same categories.

3.1 PRIMARY PREVENTION OF CWP

Primary prevention techniques are most critical in preventing disease by eliminating exposures

that lead to development of the disease. Regulatory and engineering controls are examples of

primary prevention efforts because if implemented properly they can reduce or eliminate

exposures and prevent the disease from occurring. Because there are no effective therapies for

the treatment of CWP, disease prevention through exposure reductions is the only way to

improve miners’ occupational health. Limiting exposure to coal dust through various

23

underground control measures and the appropriate enforcement of permissible limits, the Coal

Act places a strong emphasis on controlling exposures to control disease.

3.1.1 Compliance with a regulatory dust standard

Prior to federal regulations limiting coal mine dust concentrations, the average coal miner was

exposed to respirable dust in concentrations exceeding 6 mg/m3 [74]. The Coal Act established

the most stringent permissible coal dust concentration in the world at 2.0 milligrams per cubic

meter of mine air [75]. An interim standard of 3.0 mg/m3 was put into effect from 1969 to 1972,

before the two milligram standard became effective. The final standard was based primarily on

studies of United Kingdom coal miners, with the intent being the prevention of PMF by stalling

the progression of simple CWP [76]. Table 1 lists current occupational exposure limits for

respirable coal mine dust in various countries worldwide. Though there are differences in

sampling and measurement methodologies between countries, it can be seen that limit-setting

and enforcement are core principles in the primary prevention of workplace diseases worldwide

[77].

24

Table 1. Occupational exposure limits for respirable coal mine dusts worldwide (adapted from [77])

Country Dust Concentration* (mg/m3)

Australia –

Queensland

3.0

Australia - New

South Wales

2.5

Belgium 5.0

Brazil 4.0

Canada 2.0

China 6.0

Finland 2.0

Germany 4.0

India 3.0

Italy 3.3

Netherlands 2.0

Russia 2.0

South Africa 2.0

United Kingdom 3.8

United States 2.0

Turkey 5.0

* Respirable dust concentrations shown for zero silica/quartz content.

In the U.S., MSHA is responsible for establishing and enforcing the permissible exposure limit

of 2.0 mg/m3 for respirable coal mine dust (30 CFR §70.100) [78]. This dust concentration is

25

measured gravimetrically as an 8-hour TWA with a reduced standard when the respirable quartz

content exceeds 5 percent (30 CFR §70.101) [78]. Due to continued evidence of CWP in the U.S.

coal mining workforce, MSHA has recently proposed a reduction in the allowable respirable dust

concentration to 1.0 mg/m3 [79]. While this rule was first presented in 2010, MSHA has yet to

publish the final rule. Table 2 below lists these proposed regulatory exposure limits and other

recommended limits from various U.S. organizations.

Table 2. Respirable coal dust regulatory and recommended exposure limits (adapted from [80])

Exposure

Limit

mg/m3

Limit type Notes/Adjustments

MSHA (1969-1972) 3.0 8-hour TWA, PEL If SiO2 > 5%, 10 / %SiO2

MSHA (1972-

present)

2.0 8-hour TWA, PEL If SiO2 > 5%, 10 / %SiO2

MSHA (proposed) 1.0 8-hour TWA, PEL Separate standard for SiO2

ACGIH 0.9 8-hour TWA, TLV® Bituminous or lignite, separate

limit for SiO2

ACGIH 0.4 8-hour TWA, TLV® Anthracite, separate limit for

SiO2

NIOSH 1.0 10-hour TWA, REL Separate REL for SiO2

OSHA 2.4 8-hour TWA, PEL If SiO2 > 5%, 10 / (%SiO2 + 2)

CalOSHA 0.9 8-hour TWA, PEL If SiO2 > 5%, 0.1 mg/m3

Note: PEL = Permissible Exposure Limit, TLV® = Threshold Limit Value®, REL = Recommended Exposure Limit

26

Several issues are evident with the current enforcement program, most notably the lack of

cooperation between industry and government agencies. This longstanding issue can be

evidenced in the long and arduous process of developing basic regulations during the early 20 th

century as described in . Additional issues arise due to the fact that operators share responsibility

for periodic sampling of occupational dust concentrations. When collecting their samples,

operators are allowed to reduce production rates to 50 percent of the average production for the

last 5 valid samples [78]. As production has been closely linked to resulting dust concentrations

[79], this affords the mine operator the ability to intentionally reduce production during sampling

periods rather than measure dust exposures during a typical shift [81].

Weak penalties may also provide inadequate incentive for companies to take protective

measures to prevent CWP. A 2005 study found that when MSHA fines a company for violating

the relevant dust regulation, the average fine levied is only $387.85 [82]. For companies

producing millions of tons of coal annually, at an average price of $66 per ton [83], small fines

may have little financial impact.

MSHA has made efforts to address inaccurate samples and weak enforcement measures.

In 1991, MSHA revealed possible intentional mine operator tampering of dust sampling filters,

producing what were called “abnormal white centers”, so named because of the appearance of

the white filter medium in the center of the filter where black coal dust would typically be

deposited. Robert Weissman, the president of Public Citizen, called this “The Great Coal Dust

Scam” at the time [84]. Peabody Coal Company ultimately pleaded guilty to concealing the true

level of exposure to respirable dust with a $500,000 fine for tampering with dust sampling filters.

While MSHA observed a 6.5 percent proportion of invalid samples due to AWC, this reduced to

1 percent following citations and litigation [75]. As can be seen in Figure 7, the difference

27

between operator and MSHA dust concentrations was much wider in the earlier years under the

Coal Act, with the gap reduced significantly after the 1998 ruling in the case Secretary of Labor

v. Keystone Coal Mining Corp. [85].

1978

1980

1982

1984

1986

1988

1990

1992

1994

1996

1998

2000

2002

0.3

0.4

0.5

0.6

0.7

0.8

0.9

Coal

Min

e Du

st C

once

ntra

tion

(mg/

m3)

Figure 7. Operator and inspector coal mine dust measurements, 1979-2003 [14].

Even when unbiased measurements are made, infrequent sampling may allow a potentially

hazardous environment during the time between sampling events. Sampling for coal dust is only

required for five sequential shifts four times per year [78]. This frequency of sample collection is

inadequate when the variability of exposures is high. In these cases, the frequency of sample

collection must be increased to adequately estimate occupational exposure [86]. Continuous dust

sampling methods have been proposed to increase the frequency of sampling and limit the

amount of time spent under hazardous conditions. In rules proposed in 2010, MSHA requires the

use of a newly developed continuous personal dust monitor (PDM 3600) by Thermo Scientific

Inc. [79].

28

― Inspector Samples

--- Operator Samples

3.1.2 Research to develop engineering controls

The Coal Act directs a federal initiative to research means to control the dusts in underground

coal mines. The primary method to control worker exposure to coal dusts underground is to

apply ventilation and water [81]. Previously, research advancing these techniques was

undertaken by USBM, within the Department of the Interior. With the defunding and closing of

USBM in 1995 and 1996, respectively, these functions have been integrated into NIOSH’s

Office of Mine Safety and Health Research.

The research program begins at the point of dust generation and works to break the chain

leading ultimately to miner exposure. While this approach has shown to be sufficient to control

dust below permissible limits, the continuing rate of excessive exposures indicate that there are

failures in either the design or application of these controls. The NIOSH’s National Occupational

Research Agenda – Mining Sector Council has developed research objectives suggesting that

researchers develop new or improved methods of reducing miners’ exposure to dust [87].

As recently as 2005, 34 full-time employees were responsible for engineering dust

controls, developing dust monitoring techniques and instruments, and researching the monitoring

and control of diesel emissions, with a discretionary research budget of about $1.1 million [88].

A smaller portion of this workforce is dedicated to developing dust control measures for the

entire coal mining industry, with a total of 8 employees focused on continuous mining, longwall

mining, and surface coal mining. These researchers are spread among three research projects,

with a combined research budget of under $140,000 [89]. This lack of resources severely limits

the ability of researchers to devise new controls and effectively increase industry awareness to

the proper application of these controls.

29

3.2 SECONDARY PREVENTION OF CWP

Medical examinations to detect asymptomatic disease are considered to be secondary level

prevention as they allow victims to be diagnosed and treated before symptoms develop. In the

case of CWP control, screening chest x-rays and lung function tests are important to identify

disease, to evaluate the efficacy of the primary exposure control efforts, and to plan tertiary

prevention efforts of medical care and compensation.

3.2.1 Medical surveillance to track incidence and progression of CWP

Under the Coal Act, the Coal Workers’ Health Surveillance Program at NIOSH is tasked with

conducting epidemiological research to monitor the progression of CWP in the U.S. labor force.

This approach to disease control can be termed secondary prevention, with the goal being to

identify and treat the disease before symptoms develop. The Coal Act specifies that each coal

mine operator offer an initial chest radiograph to every newly employed underground miner and

then again approximately every five years. When a U.S. coal miner dies, the Coal Act also

allows for families to arrange for a free autopsy to both help support a potential benefit claim and

to provide scientists with more detailed information about CWP.

At the onset of the National Study of Coal Workers’ Pneumoconiosis in 1969, the

prevalence of CWP in bituminous miners was estimated to be 47 percent [20]. Subsequent work

by NIOSH technicians in the Coal Workers’ X-ray Surveillance Program (CWXSP) observed

lung damage in 30 percent of examined individuals [24]. As discussed previously, until recently

the rate of CWP in the U.S. workforce was declining. First noted around 2000, NIOSH

researchers have observed an increased prevalence of CWP, especially in localized regions of the

30

Appalachian coalfields. These findings caused NIOSH to augment coal worker surveillance

efforts through enhanced surveillance, called the Enhanced Coal Workers’ Health Surveillance

Program (ECWHSP). This program, in addition to a similar initiative by MSHA, sought to

increase levels of participation in “hot spot” regions by deploying mobile examination units

(Figure 8).

Figure 8. NIOSH CWXSP mobile examination unit.

Some issues have been raised with the current approach to surveillance. For example, because of

the voluntary nature of these exams, various forms of ascertainment bias may be present, with

some members of the miner population being more, or less, likely to be included than others. As

an example of a self-selection bias, workers who are experiencing symptoms or fears of

respiratory distress may be more likely to seek medical examination than those that are non-

symptomatic. This could result in rates of CWP being skewed higher than reality. Another

potential issue is a healthy worker effect, in which some workers, who have become disabled or

died, cannot or do not participate in the screening process. These sick or deceased individuals are

not included in the official tally. While the recruitment efforts by the ECWHSP have increased

participation rates, concerns about oversampling in certain regions have led some researchers to

suggest that the results from the ECWHSP be separated from the base findings of the CWXSP

31

[90]. NIOSH has acknowledged these biases, finding that these tended to underestimate the true

burden of disease among underground coal miners [91].

Not all miners exercise their right to free examinations when they are available. Though

the rate of participation has been continuously increasing over each five-year sampling period

since 1990, less than half of all miners receive medical screening at least once during the period

[24]. This poor participation rate may be attributed to external factors that influence the miners’

willingness to take advantage of voluntary medical exams. For example, in Kentucky, there is a

short period of time available following diagnosis for miners to seek compensation for their

work-related illness, with compensatory claims required to be filed within three years after

diagnosis. Many workers, who are not experiencing any symptoms from their disease and are not

permitted to receive benefits while they are still employed may not want to seek these benefits

and possibly lose their much larger mining paychecks [92]. Finally, although 30 CFR §90

provides job reassignments without loss of regular pay to miners exhibiting CWP (described in

more detail in 3.3.2), many miners are reluctant to submit to the medical surveillance and

potentially lose the overtime income that regular miners frequently earn.

3.3 TERTIARY PREVENTION OF CWP

Tertiary prevention targets victims of the disease and attempts to slow progression of the disease.

This can include treatment, job reassignment, compensation, and rehabilitation to improve

quality of life and prevent complications from the disease. The Coal Act aims to achieve this by

providing access to care and financial benefits through a worker compensation scheme while

also offering reassignment to less hazardous work locations.

32

3.3.1 Compensation for disease and disability

In 1946 contract negotiations, following a long strike and ultimate government seizure of the

nation’s coal mines, John L. Lewis, the president of the United Mine Workers of America

(UMWA), pushed for direct compensation of occupational diseases. He made this demand with

the realization that proposed prevention efforts would likely never be achieved. Eventually

signed at the White House, the new contract established the Welfare and Retirement Fund (now

UMWA Health and Retirement Funds), providing for miners in the cases of sickness, disability,

death, or retirement. This fund was initially financed by a royalty of 5 cents per ton of coal

produced, increasing to 10 cents in the subsequent National Bituminous Coal contract of 1947.

This fund would not only change the way in which miners and their diseases were viewed by the

medical community and the public at large, this approach to compensation would change the

way that employees in other industries were repaid for harm caused by their occupational

exposures [93].

Continuing the compensation movement begun in the 1940’s and bowing to efforts from

the newly formed Black Lung Association [94], the federal government mandated a federal

system of worker’s compensation in the 1969 Coal Act. Title IV of the Coal Act established the

Federal Black Lung Benefits Program, providing relief to state workers’ compensation programs

and the estimated 125,000 miners, both UMWA-affiliated and non-union, suffering from

pneumoconiosis at the time [94]. The program, initially administered by the Social Security

Administration, provided compensation with public funds for those victims of coal mine dust

exposure.

By the early 1970’s, with the number of claims far exceeding expectations, changes were

made by the Black Lung Benefits Act of 1972 in eligibility criteria to streamline the claim

33

process. Further changes were made in the Black Lung Benefits Reform Act of 1977 to help to

resolve the ongoing problem of outstanding and unapproved claims.

The Black Lung Disability Trust Fund (BLDTF), established by the Black Lung Benefits

Revenue Act of 1977, was created to provide initial benefits, financed by excise taxes on coal

produced by both surface and underground methods, at rates of $0.50 and $1.10 per ton,

respectively. These taxes continue to provide revenues of approximately $566 million annually

[95]. Currently, over 25,000 beneficiaries receive monthly federal payments ranging from about

$625 to $1,250 for their disability [96], [97], with the BLDTF reporting a negative balance of

$6.1 billion [98].

Despite the availability of federal benefits, miners face substantial barriers to accessing

compensation from the BLDTF. One major hurdle is initially proving that the miner has black

lung, as defined by the law. A recent Government Accounting Office (GAO) report showed that

for 2008, the Department of Labor (DOL) denied 87 percent of claims [99]. This rate of denial is

attributed to the influence on DOL administrative law judges by the weight of evidence

presented by mining companies, whose doctors have much more familiarity with the disease than

individual miners’ doctors. The same GAO report found that 4 percent of the 763 miners who

gained black lung benefits between 2001 and 2008 waited up to 8 years for their awards. While

the bulk of the awards (73 percent) were received within three years, nearly one quarter of the

cases took between three and six years. This delay and denial in receiving benefits brings into

question the efficiency of the compensation program.

The credibility of the program has been challenged by a 2013 joint investigation by ABC

News and the Center for Public Integrity. The investigators found that Dr. Paul Wheeler, a doctor

and professor of radiology at Johns Hopkins Hospital, had not once observed the severe form of

34

the disease since 2000, despite reviewing over 1500 CWP x-rays [100]. Although Johns Hopkins

subsequently suspended their x-ray review program, Dr. Wheeler’s findings have resulted in the

denial of benefits to numerous miners and their families [101].

3.3.2 Medical removal and job reassignment

Part 90 of the Coal Act establishes an occupational reassignment program to identify miners with

medical evidence of CWP and remove them to less dusty environments (30 CFR §90) [78]. This

was the first mandated medical removal protection program proposed by the federal government

[102]. The dust exposure limit is reduced to 1.0 mg/m3 for those participating in the voluntary

program, with more frequent sampling required (30 CFR §90.100 and 30 CFR §90.208,

respectively) [78]. Acknowledging that the disease may continue to progress following transfer,

this reduction in dust exposure is intended to slow the progression of disease while still

providing wage and job protection [30]. The Coal Act specifies that a Part 90 miner “shall

receive compensation for such work at not less than the regular rate of pay received by him

immediately prior to his transfer.” Despite these protections, less than 15 percent of eligible

miners exercise their medical removal rights [103]. This lack of participation calls into question

both the framework and execution of the system in achieving worker protection in the U.S. coal

mines.

Both lack of awareness and confusion about the program have been cited as reasons for

poor participation rates [104]. As previously discussed, less than fifty percent of coal miners

participate in the CWXSP. Because individuals eligible for Part 90 transfer are notified following

examination by NIOSH’s CWXSP, those miners that do not participate in the CWXSP will not

be informed to participate in the Part 90 program. While it is possible for a miner to be examined

35

independently at an approved facility, at his own expense, this is likely a barrier to participation

in the program.

Another factor in low participation rates may be the lack of economic diversity in the

nation’s coalfields. As alternative well-paying employment opportunities are scarce, workers are

less inclined to call attention to themselves by asserting their rights under the Coal Act. Although

Part 90 miners must be moved to jobs with lower dust concentration, this transfer itself may keep

some from participating. For example, upon exercising the option for relocation, “a Part 90

miner is not entitled to dictate to the operator or otherwise specify the particular position to

which the transfer must be made.” [105]. This lack of choice in assignment may result in the

miner being assigned to what may be considered to be an inferior position, losing the opportunity

for production incentives and overtime pay. Until more eligible miners are engaged in this

program, the positive impact on disease progression and overall health status will be limited.

36

4.0 RECOMMENDATIONS

Although rates of CWP have declined substantially following the 1969 passage of the Coal Act,

recent evidence shows that the decline has ended. In order to fully eliminate the disease, renewed

efforts and alternative approaches may be necessary. To this end, MSHA published a proposed

rule in 2010 to reduce the permissible dust exposure limit and modify sampling strategies. Even

with these proposed changes, the new dust rules overlook some issues in preventing new cases of

CWP.

The current system of CWP control in U.S. coal mines employs a diversified approach of

enforcement, engineering, medical surveillance, and compensation. Upon critical review, several

components of this system have significant flaws that may detract from the goal of protecting

coal miners. A recent increase observed in the rate of CWP in coal miners is likely multifactorial

and indicates possible failures in one of more parts of the system. Possible explanations include

excessive exposures and undetected toxicities associated with these exposures. The following

recommendations arise due to the continued risk of CWP in the nation’s mines.

4.1 IMPROVED DUST MONITORING AND CONTROL

The current MSHA sampling regime generates over 100,000 personal samples each year. NIOSH

has questioned if these samples could be better collected to ensure that the exposure of every

37

coal miner is below the dust limit for every shift [15]. Even with demonstrated compliance to the

current regulations, the opportunity exists for miners to be overexposed for long intervals

between sampling activities. Increasing the sampling frequency and requiring representative

rates of coal production will improve the link between sample results and true coal dust

exposures. Increased sampling frequency will also prevent mine operators from temporarily

modifying the mine environment to produce lower dust levels, through ventilation changes or

other transitory conditions. These frequent samples will also provide rapid assessment of the

mine atmosphere to identify when significant changes in either dust generation or exposure

controls occur. This is especially important in working areas of underground coal mines where

conditions can change very quickly.

When mines identify conditions that present a hazard to miners that may result in

overexposure to coal dust, engineering controls or modified work practices must be implemented

promptly. For operators and miners to make these changes, proven and reliable interventions

must be available. Continued research into engineered dust controls, safe work practices,

respiratory protections, dust characteristics, and health effects is essential to developing state-of-

the-art technologies and controls. Sufficient resources, in terms of both personnel and funding,

are needed to advance current designs and promote new approaches to dust control.

4.2 TARGETED INTERVENTIONS

In order to reduce the burden of CWP, interventions must address the factors tied most closely to

the incidence of disease. Controlling exposures to excessive concentrations of coal mine dust and

minimizing total lifetime dust burdens appear to be the best means to preventing CWP. As has

38

been shown by many epidemiological studies, when there is little exposure to dust, there is a low

probability of respiratory illnesses, including CWP. Efforts to reduce overall dust concentrations

will have the direct effect of lowering exposures and reducing rates of CWP. This should be the

primary focus of all parties involved: regulators, operators, miners, and researchers.

A targeted approach would also focus on coal mines that have a history of violations and

are associated with risk factors for CWP. As the rates of CWP appear to be higher in smaller

mines and in mines located in the Central Appalachian Region, resources may be best allocated

to these operations. Although the mines located in the Central Appalachian Region demonstrate

lower levels of non-compliance to current dust regulations, they are associated with rates of

CWP far in excess to the rest of the coal mining industry. Efforts by NIOSH and MSHA to

enhance worker surveillance in this region address only secondary prevention to CWP.

Engineering controls, work plans, and enforcement practices should be specifically developed

for the potentially unique mining conditions to prevent hazardous exposures.

Efforts must also be focused on improving protections at small mines. Elevated rates of

CWP and PMF at small mines demonstrate higher levels of exposure. Improved surveillance and

sampling in this region should work to quantify exposures and identify the presence of any

unique toxicities. If small mines lack the resources to provide effective worker protection,

technical assistance may help in identifying cost-effective dust controls and improving

management of respiratory protection programs.

While the current regulations strive to reduce exposures to dust, there remain apparent

excess risks when exposed to current dust levels. As has been suggested by ACGIH, different

dust concentration limits for different dust compositions may be appropriate. In areas with coal

39

dust exhibiting especially toxic qualities due to coal rank or iron content, interventions may be

developed to address these conditions.

4.3 MINER ENGAGEMENT AND PARTICIPATION

In order to realize Congress’s stated goal to “adequately assure that no miner would suffer

material impairment of health or functional capacity even if exposed to the regulated substance

or hazard regularly for the period of his working life” [102], individual miners must play a role

in engaging in protective behaviors and participating in medical surveillance programs.

Improved communication about the hazards, including the potential health effects and modern

tools to measure exposure should be included in both new miner training (30 CFR §48.5) and in

annual refresher training of miners (30 CFR §48.8) [78]. NIOSH has developed education and

training materials to be used in these settings. One particular product, “Faces of Black Lung”,

provides first-hand accounts from two victims of CWP, showing how the disease has changed

their lives and their relationships with loved ones [106].

There continues to be a disconnection between behaviors and health effects due to the

delay between dust exposure and onset of CWP. Recent efforts by NIOSH and MSHA have

increased participation in medical surveillance programs, but still fail to engage about half of all

coal miners. NIOSH has emphasized continued communication about “the purposes of the

medical screening and surveillance program, the health-protection benefits of participation, and a

description of the procedural aspects of the program” [15]. While this may be effective, this

information may be best delivered to miners by other miners using their own words, as in the

40

video “Faces of Black Lung”. It is suggested that current and former miners be enlisted to

provide this information to fellow miners for maximum impact.

New dust measuring instruments can provide miners with more prompt feedback about

exposures and cues for action than prior methods, like gravimetric measurements, which provide

results days later. Following introduction and training, the continuous feedback from the PDM

3600 personal dust monitor has been shown to encourage miners to modify their behaviors and

lower dust exposures [107]. Although first priority should be given to implementing engineering

controls for coal dust, this PDM feedback may also increase respirator usage for miners in work

areas contaminated by coal dust.

4.4 INSTITUTIONAL REFORM

Another issue with the current approach to CWP prevention in U.S. coal mines is the lack of

incentives afforded to mine operators for innovation. For example, the current disease

compensation program fails to reward innovation or implementation of industry-accepted best

practices for worker dust protection. Developing an incentive system for mines that take

proactive steps and thereby reduce their liability to coal excise taxes would reward proactive

behaviors that address the primary means of CWP prevention. A similar, comprehensive risk-

based framework to mine safety and health has been proposed by the National Mining

Association [108].

41

5.0 CONCLUSIONS

When miners enter the U.S. coal mining workforce, they should expect to work a full career with

no negative health effects. Although the prospects are better than they were forty years ago, this

is not currently the case for CWP. Improvements of many aspects of the current respirable dust

control program have been proposed: reduced respirable dust concentration limits [15], targeted

research [87], improved enforcement and compliance [79], [81], and overhauled compensation

and benefits programs [99]. To date, few of these suggestions have been effectively

implemented, with CWP rates increasing in recent health surveys.

Evidence from Australia’s coal fields indicates that a very low level of disease incidence

can be attained even with a higher permissible dust concentration and associated dust exposures

[109]. This has implications for the U.S., suggesting that a unique property of U.S. coal exposure

is responsible for causing observed rates of CWP. NIOSH researchers have proposed that quartz

exposures, extended shift lengths, and potential bias in compliance sampling may be key factors

in the recent resurgence of CWP [30]. The present analysis bears this out, showing that

environmental factors such as mass concentration and mine location can have major effects on

individual risks of CWP.

Any effort to reduce the rates of CWP must first focus on improving the work

environment. The Federal Coal Mine Health and Safety Act of 1969 established environmental

dust standards for underground coal mines, requiring that the concentration of respirable dust in

42

the mine atmosphere not exceed 2.0 mg/m3 for a working shift [78]. Coal mine operators

currently demonstrate a high level of compliance to these dust regulations. In the face of

continued evidence of CWP in the workforce, MSHA has published a proposed dust rule that

contains several changes including lowering the coal mine dust standard to 1.0 mg/m3, increasing

the frequency of compliance dust sampling, utilizing a single sample to determine compliance,

and requiring the use of a continuous personal dust monitor for compliance sampling [79]. This

approach by MSHA acknowledges that simply choosing a lower allowable dust concentration

does not ensure that CWP will be reduced or eliminated. By modifying the associated sampling

strategy, MSHA hopes to reduce bias in sampling and time spent exposed to elevated dust

concentrations. MSHA’s risk assessment estimates that these changes will significantly reduce

the risks of CWP and other respiratory diseases [79].

External factors, including geography and mine size, also play a role in a miner’s lifetime

risk of developing CWP. The distribution of CWP occurrence is not distributed uniformly across

the nation and all coal mining operations. Small mines and mines located in the Central

Appalachian region present higher risks of CWP. Current and proposed dust rules do not contain

provisions for small mines or specific regions. If permissible dust concentrations are reduced,

this omission may have potential effects similar to those seen for the Coal Act, with the resulting

closure of numerous small or marginal coal mines [110]. While this will eliminate some of the

smaller mines associated with high rates of CWP, it will also produce a concentrated regional

economic impact in the nation’s coal fields.

Finally, miners are integral parts of any dust control program. They should be aware of

the hazards of overexposure to respirable coal dust, engineering controls to mitigate these

hazards, and medical interventions available for their benefit. Training should focus on providing

43

plain language explanations and encouragement to participate in surveillance efforts. As the

beneficiaries of the dust program and ultimate bearers of potential negative health effects from

any failures, miners must avail themselves of protections underground (i.e. engineering controls

and respirators) and early detection of disease and take an active role in protecting their personal

health status. Through these interventions, the promise of a fulfilling career with no health

impairments may be realized.

What’s on your face, you can wash off, but what’s on your lungs, you can’t.

– Carl L. Bailey, “Face of Black Lung”

44

APPENDIX A: DEVELOPMENT OF THE TERMINOLOGY OF COAL WORKERS’

OCCUPATIONAL LUNG DISEASES

Exposure to airborne particulate matter has long been known to be a serious health threat to

workers in many industries. In coal mining, overexposure to respirable coal mine dust particles

can lead to the breathing distress that comes by many names: black lung, miners’ asthma,

miners’ consumption, coalworkers’ cough, anthracosis, or pneumoconiosis [111]. Most of these

terms can be traced back to a specific time period, where doctors and the miners themselves

classified the disease using the “terminology of the day” [112].

One of the first modern medical reports to comment on the unusual respiratory disease

burden of coal miners was brought by Dr. W. Marshall in 1825 [113]. Described as “phthisis

melatonica,” this “pigmented wasting disease” was observed in the lungs of Welsh coal miners

who “attributed the commencement of ailments to having wrought for some time in a very

impure atmosphere.” In 1831, the specific lung diseases of coal miners in Great Britain were

termed “Miners’ Black Lung” by physician Dr. J.C. Gregory, who arrived at this term from the

black masses found in the lungs of a deceased miner [114]. Shortly thereafter, in 1838, a Scottish

doctor by the name Dr. Thomas Stratton suggested the use of the term “anthracosis” to describe

the same condition [115]. The more general term “pneumoconiosis” was later introduced by

German pathologist and physician Friedrich von Zenker in 1866 to describe “dusty lungs” that he

observed over a range of occupations, not just coal mining [116].

Official governmental terminology for the miners’ unique and debilitating disease

condition developed in the 1940s when a national British compensation program, the Coal

Mining Industry (Pneumoconiosis) Compensation Scheme, 1943, provided disability

45

determinations of “coal miner’s pneumoconiosis” to disabled workers. This phrase was later

updated to “coal workers’ pneumoconiosis”, taking into consideration that many other coal

handlers and processors were succumbing to the disease, not just those that toiled in the mines.

This is the term adopted by the U.S. medical establishment for disease detection, diagnosis, and

treatment [117].

In the U.S., the phrase “black lung” is both colloquial and legal in nature, not a strict

medical diagnosis or classification of respiratory dysfunction. Barbara Ellen Smith extensively

describes the social and political struggle to control and widen the definition of “black lung”

[118]. The late 1960’s movement fostered by the Black Lung Association was a direct challenge

to the medical establishment which had previously attributed the disease to weak constitution,

poor living conditions, individual habits (e.g. smoking), and fear of the mines rather than a

contaminated work atmosphere. By defining the nature of the disease as both occupational and

abnormal, miners and their advocates played a considerable role in the approach to control and

prevent dust exposures, and compensate affected victims. The Federal Mine Safety and Health

Act of 1977 (Public Law 91-173) broadly defined the term “black lung” as “a chronic dust

disease of the lung arising out of employment in an underground coal mine.” Miners falling

under this definition may be compensated for their disability by the Black Lung Disability Trust

Fund. This compensation program is explored in section 3.2. Even today, the definition of black

lung continues to be debated, with some coal companies asserting a narrow view that applies

only to the classical presentation of the lung disease as opacities appearing on x-ray film and not

one of the other medically-recognized manifestations of disease, like loss of lung capacity,

emphysema, or chronic bronchitis [100].

46

APPENDIX B: BRIEF HISTORY OF U.S. MINING HEALTH AND SAFETY

REGULATION TO 1969

From the early years of the United States, coal miners have been subjected to occupational

hazards that have tragically shortened their lives, in both sudden and prolonged manners. From

the major mine fires and explosions where over 400 men and boys perished to the working air

frequently contaminated with coal dust and noxious gases, history is replete with stories of the

risks encountered by those who extracted, processed, and used coal. Prior to the first Federal

safety regulations in 1910, states were largely independent in their oversight of the mining

industry, with some states enacting their own legislation to ensure safer working conditions.

Most of these controls were put into place to protect the miners from explosion and fire, rather

than to specifically prevent occupational injuries and diseases.

Following a string of major mine disasters, most notably the Monongah disaster of

December 6, 1907, where 361 miners died from a coal dust-fueled explosion, Congress

established the U.S. Bureau of Mines (USBM). In the years from 1910 to 1941, the USBM had

minimal influence on the health and safety at individual mines, due to a lack of authority and

insufficient funding. In 1940, with a staggering 1,388 miners killed in numerous disasters and

accidents, public pressure mounted for improved working conditions [17]. The Federal Coal

Mine Safety Act of 1941 (Public Law 49) attempted to improve federal oversight by providing

inspectors with the right of entry to the nation’s coal mines, though they did not yet have any

specific health or safety standards to enforce.

47

The USBM would continue in this advisory role until 1952, when the Federal Mine

Safety Act (Public Law 82-522) would allow federal inspectors to issue notices of violation and

orders of withdrawal to mines employing more than 15 underground miners. Unfortunately, this

change produced very little effect on the rate of fatalities in U.S. coal mines with the rates

continuing to stagnate (Figure 9). The mines in the U.S. remained the most dangerous in the

developed world, with death rates far exceeding those in other developed countries, like France,

Belgium, Great Britain, and Netherlands. Only once from 1951 to 1965 did another nation’s

fatality rate exceed that of the U.S., with West Germany suffering 1.60 fatalities per 100,000

hours worked in 1962 [110]. This anomalous rate in West Germany was the result of the horrific

Luisenthal Mine disaster, a series of explosions killing 299 of the 433 miners underground [119].

1900 1910 1920 1930 1940 1950 19600

500

1,000

1,500

2,000

2,500

3,000

3,500

0

1

2

3

4

5

6

Fatalities

Rate

Num

ber o

f Fat

aliti

es

Fata

lity

Rate

Figure 9. Fatalities at U.S. coal mines, 1900-1969 [17].

In a recurrence of the past, a major U.S. disaster in 1968 renewed the call for increased mine

safety regulations. A November 20th blast killed seventy-five miners and three federal inspectors

48

in Farmington, West Virginia. A hoard of news media traveled to the area, investigating the

background for their stories. Though they gained little insight from the mining company officials

during this time, they did observe widespread respiratory disorders in those they contacted in the

industry. To capitalize on the attention and to elevate health issues to the same level as other

safety issues, the Black Lung Association was formed in January 1969. Concern with the lack of

protections and benefits for those suffering from black lung disease frequently resulted in

“wildcat strikes” (work stoppages not sanctioned or sponsored by the United Mine Workers of

America) and demonstrations throughout the U.S. coal fields [94]. These decidedly political

actions would have a profound effect on the resulting legislation, the Federal Coal Mine Health

and Safety Act of 1969 (the Coal Act), especially in the establishment of compensatory benefits.

The Coal Act is detailed in greater detail beginning in Chapter 3.0 .

49

BIBLIOGRAPHY

[1] J. K. Corn, "Historical aspects of industrial hygiene--II. Silicosis," Journal of

American Industrial Hygiene Association, vol. 41, no. 2, pp. 125-133, 1980.

[2] Strabo, The Geography of Strabo, H. L. Jones, Ed., Cambridge, MA: Harvard

University Press, 1924.

[3] G. Agricola, De Re Metallica, Translated from the First Latin Edition of 1556, H. C.

Hoover and L. H. Hoover, Eds., London: Mining Magazine, 1912.

[4] D. W. Dockery, C. A. Pope, X. Xu, J. D. Spengler, J. H. Ware, M. E. Fay, B. G.

Ferris and F. E. Speizer, "An association between air pollution and mortality in

six U.S. cities," New England Journal of Medicine, vol. 329, no. 24, pp. 1753-

1759, 1993.

[5] D. S. Shprentz, G. C. Bryner and J. S. Shprentz, "Breath-taking: Premature mortality

due to particulate air pollution in 239 American cities," Natural Resources

Defense Council, Washington, DC, 1996.

[6] D. Abbey, N. Nishino, W. McDonnell, R. Burchette, S. Knutsen, W. Beeson and J.

Yang, "Long-term inhalable particles and other air pollutants related to

mortality in nonsmokers," American Journal of Respiratory and Critical Care

50

Medicine, vol. 159, no. 2, pp. 373-382, 1999.

[7] F. Dominici, A. McDermott and M. Daniels, "Mortality among residents of 90 cities,"

in Revised analyses of time-series studies of air pollution and health,

Montpelier, VT, Capital City Press, 2003.

[8] I. M. Kennedy, "The health effects of combustion-generated aerosols," Proceedings

of the Combustion Institute, vol. 31, no. 2, pp. 2757-2770, 2007.

[9] D. W. Dockery and C. A. Pope, "Acute respiratory effects of particulate air

pollution," Annual Review of Public Health, vol. 15, pp. 107-132, 1994.

[10] Environmental Protection Agency, "National Trends in Particulate Matter Levels,"

2013. [Online]. Available: http://www.epa.gov/airtrends/pm.html. [Accessed

October 2013].

[11] U.S. Bureau of the Census, "Historical Statistics of the United States, Colonial Times

to 1970, Part 1," U.S. Department of Commerce, Washington, DC, 1975.

[12] EIA, "Annual Coal Report, 2012, Table 21. Coal Productivity by State and Type,"

2012. [Online]. Available: http://www.eia.gov/coal/annual/pdf/table21.pdf.

[Accessed December 2013].

[13] D. Lockard, Coal: A Memoir and Critique, Charlottesville: University Press of

Virginia, 1999.

[14] NIOSH, "Work-Related Lung Disease Surveillance System (eWoRLD): Coal

Workers' Pneumoconiosis: Coal Dust Exposures," 28 March 2013. [Online].

Available: http://www2a.cdc.gov/drds/worldreportdata/SubsectionDetails.asp?

ArchiveID=1&SubsectionTitleID=7. [Accessed October 2013].

[15] NIOSH, Criteria for a recommended standard: Occupational exposure to coal mine

51

dust, DHHS (NIOSH) Publication No. 95-106, Washington, DC: U.S.

Department of Health and Human Services, Public Health Service, Centers for

Disease Control and Prevention, National Institute for Occupational Safety and

Health, 1995.

[16] MSHA, "Mine Safety and Health at a Glance," 30 June 2013. [Online]. Available:

http://www.msha.gov/mshainfo/factsheets/mshafact10.pdf. [Accessed October

2013].

[17] MSHA, "Mine Safety and Health Administration - Mining Industry, Accident,

Injuries, Employment, and Production Statistics," 2010. [Online]. Available:

http://www.msha.gov/ACCINJ/BOTHCL.HTM. [Accessed October 2013].

[18] NIOSH, "Work-Related Lung Disease Surveillance System (eWoRLD): Reference

Number 2012F02-01," 28 March 2013. [Online]. Available:

http://www2a.cdc.gov/drds/worldreportdata/FigureTableDetails.asp?

FigureTableID=2568&GroupRefNumber=F02-01. [Accessed October 2013].

[19] J. F. Colinet, J. P. Rider, J. M. Listak, J. A. Organiscak and A. L. Wolfe, Best

Practices for Dust Control in Mining, DHHS (NIOSH) Publication No. 2010-

110, Information Circular 9517, Pittsburgh, PA: U.S. Department of Health

and Human Services, Public Health Service, Centers for Disease Control and

Prevention, National Institute for Occupational Safety and Health, 2010, pp. 1-

76.

[20] W. K. C. Morgan, R. Reger, D. B. Burgess and E. Shoub, "A comparison of the

prevalence of Coal Workers' Pneumoconiosis and respiratory impairment in

Pennsylvania bituminous and anthracite miners," Annals of the New York

52

Acadamy of Science, vol. 200, pp. 252-259, 1972.

[21] ILO, "Guidelines for the use of ILO international classification of radiographs of

pneumoconiosis. Revised edition. Occupation Safety and Health Services No.

22," International Labour Office, Geneva, Switzerland, 1980.

[22] A. Seaton, N. L. Lapp and W. K. C. Morgan, "The relationship of pulmonary

impairment in simple coal workers' pneumoconiosis to type of radiographic

opacity," British Journal of Industrial Medicine, vol. 29, pp. 50-55, 1974.

[23] B. G. Miller and M. Jacobsen, "Dust exposure, pneumoconiosis, and mortality of

coalminers," British Journal of Industrial Medicine, vol. 42, no. 11, pp. 723-

733, 1985.

[24] NIOSH, Work-Related Lung Disease Surveillance Report 2002, DHHS (NIOSH)

Publication Number 2003-111, U.S. Department of Health and Human

Services, Public Health Service, Centers for Disease Control and Prevention,

National Institute for Occupational Safety and Health, 2003, pp. 1-246.

[25] E. Storey and A. Laney, "Respiratory disease in US coal miners," in Preprints of

2014 SME Annual Meeting and Exhibit, Salt Lake City, 2014.

[26] J. D. McAteer, K. Beall, J. A. Beck, P. C. McGinley, C. Monforton, D. C. Roberts, B.

Spence and S. Weise, Upper Big Branch, The April 5, 2010 Explosion: A

Failure of Basic Coal Mine Safety Practices, 2011.

[27] NIOSH, "Work-Related Lung Disease Surveillance System (eWoRLD): Coal

Workers' Pneumoconiosis: Morbidity," April 2011. [Online]. Available:

http://www2a.cdc.gov/drds/WorldReportData/FigureTableDetails.asp?

FigureTableID=2550&GroupRefNumber=T02-12. [Accessed October 2013].

53

[28] D. E. Pollock, J. D. Potts and G. J. Joy, "Investigation into dust exposures and mining

practices in mines in the Southern Applachian Region," in SME Annual

Meeting and Exhibit, February 22-25, Denver, Colorado, Littleton, CO, 2009.

[29] E. Suarthana, A. S. Laney, E. Storey, J. M. Hale and M. D. Attfield, "Coal workers'

pneumoconiosis in the United States: regional differences 40 years after

implementation of the 1969 Federal Coal Mine Health and Safety Act,"

Occupational and Environmental Medicine, vol. 68, no. 12, pp. 908-913,

2011.

[30] V. C. Antao, E. L. Petsonk, L. Z. Sokolow, A. L. Wolfe, G. A. Pinheiro, J. M. Hale

and M. D. Attfield, "Rapidly progressive coal workers' pneumoconiosis in the

United States: geographic clustering and other factors," Occupational and

Environmental Medicine, vol. 62, pp. 670-674, 2005.

[31] M. Jacobsen, S. Rae, W. H. Walton and J. M. Rogan, "The relation between

pneumoconiosis and dust exposure in British coal mines," in Inhaled particles

III, Old Woking, England, Unwin Brothers, 1971, pp. 903-919.

[32] M. D. Attfield and K. Morring, "An investigation into the relationship between coal

workers' pneumoconiosis and dust exposure in U.S. coal miners," American

Industrial Hygiene Journal, vol. 53, no. 8, pp. 486-492, 1992.

[33] V. Vallyathan, D. P. Landsittel, E. L. Petsonk, J. Kahn, J. E. Parker, K. T. Osiowy

and F. H. Y. Green, "The influence of dust standards on the prevalence and

severity of coal worker's pneumoconiosis at autopsy in the United States of

America," Archives of Pathology & Laboratory Medicine, vol. 135, no.

December, pp. 1550-1556, 2011.

54

[34] A. D. Maynard and R. J. Aitken, "Assessing exposure to airborne nanomaterials:

current abilities and future requirements," Nanotoxicology, vol. 1, pp. 26-41,

2007.

[35] C. Monteiller, L. Tran, W. MacNee, S. Faux, A. Jones, B. Miller and K. Donaldson,

"The pro-inflammatory effects of low-toxicity low-solubility particles,

nanoparticles and fine particles, on epithelial cells in vitro: the role of surface

area," Occupational and Environmental Medicine, vol. 64, no. 9, pp. 609-615,

2007.

[36] N. S. Seixas, P. Hewett, T. G. Robins and R. Haney, "Variability of particle size-

specific fractions of personal coal mine dust exposures," American Industrial

Hygiene Association Journal, vol. 56, no. 3, pp. 243-250, 1995.

[37] J. D. Potts, M. A. McCawley and R. A. Jankowski, "Thoracic dust exposures on

longwall and continuous mining sections," Applied Occupational and

Environmental Hygiene, vol. 5, pp. 440-447, 1990.

[38] W. A. Kerby, J. R. Lakey and R. J. Sarjant, "A study of coal extracts by infrared

spectroscopy," Fuel, vol. 33, p. 480, 1954.

[39] R. A. Meyers, Coal Structure, New York: Academic Press, Inc., 1982.

[40] H. M. Braunstein, E. D. Copenhaver and H. A. Pfuderer, "Environmental Health and

Control Aspects of Coal Conversion: An Information Overview, Report

ORNL-EIS-94," Oak Ridge National Laboratory, Oak Ridge, TN, 1977.

[41] X. Huang, W. H. Li, M. D. Attfield, A. Nadas, K. Frenkel and R. B. Finkelman,

"Mapping and prediction of coal workers’ pneumoconiosis with bioavailable

iron content in the bituminous coals," Environmental Health Perspectives, vol.

55

113, pp. 964-968, 2005.

[42] R. J. McCunney, P. Morfeld and S. Payne, "What component of coal causes coal

workers' pneumoconiosis?," Journal of Occupational and Environmental

Medicine, vol. 51, no. 4, pp. 462-471, 2009.

[43] M. D. Attfield and N. S. Seixas, "Prevalence of pneumoconiosis and its relationship

to dust exposure in a cohort of U.S. bituminous coal miners and ex-miners,"

American Journal of Industrial Medicine, vol. 27, pp. 137-151, 1995.

[44] M. D. Attfield and T. K. Hodous, "Pulmonary function of U.S. coal miners related to

dust exposure estimates," American Journal of Public Health, vol. 143, no. 3,

pp. 605-609, 1992.

[45] J. F. Hurley and W. M. Maclaren, "Dust-Related Risks of Radiological Changes in

Coalminers Over a 40-Year Working Life: Report on Work Commissioned by

NIOSH, IOM Report No. TM/87/09," Institute of Occupational Medicine,

Edinburgh, 1987.

[46] ACGIH, 2013 TLVs and BEIs, Cincinnati, Ohio: American Conference of

Governmental Industrial Hygienists, 2013.

[47] A. G. Heppleston, "Prevalence and pathogenesis of pneumoconiosis in coal workers,"

Environmental Health Perspectives, vol. 78, pp. 159-170, 1988.

[48] NIOSH, "Coal mine dust exposures and associated health outcomes: A review of

information published since 1995," in Current Intelligence Bulletin 64,

Washington, DC, U.S. Department of Health and Human Services, Public

Health Service, Centers for Disease Control and Prevention, National Institute

for Occupational Safety and Health, 2011, pp. 1-38.

56

[49] I. C. White, "Stratigraphy of the Bituminous Coal Field of Pennsylvania, Ohio, and

West Virginia: Bulletin of the United States Geological Survey, Number 65,"

U.S. Department of the Interior, U.S. Geological Survey, Washington, D.C.,

1891.

[50] J. L. Lancaster, "Coal mine characteristics associated with progressive coal worker's

pneumoconiosis," Walden University, Minneapolis, MN, 2011.

[51] D. A. Scarisbrick and T. R. Quinlan, "Health surveillance for coal workers'

pneumoconiosis in the United Kingdom, 1998-2000," Annals of Occupational

Hygiene, vol. 46, no. Suppl. 1, pp. 245-256, 2002.

[52] A. J. Ghio and D. R. Quigley, "Complexation of iron by humic-like substances in

lung tissue: role in CWP," American Journal of Physiology, vol. 267, pp.

L173-L179, 1994.

[53] A. D. Harrington, S. E. Tsirka and M. A. Schoonen, "Inflammatory stress response in

A549 cells as a result of exposure to coal: Evidence for the role of pyrite in

coal workers’ pneumoconiosis pathogenesis," Chemosphere, vol. 93, pp. 1216-

1221, 2013.

[54] C. E. Rossiter, "Relation between content and composition of coal workers' lungs and

radiological appearances," British Journal of Industrial Medicine, vol. 29, pp.

31-44, 1972.

[55] A. S. Laney and M. D. Attfield, "Coal workers' pneumoconiosis and progressive

massive fibrosis are increasingly more prevalent among workers in small

underground coal mines in the United States," Occupational and

Environmental Medicine, vol. 67, no. 6, pp. 428-431, 2010.

57

[56] W. A. Wade, E. L. Petsonk, B. Young and I. Mogri, "Severe occupational

pneumoconiosis among West Virginian coal miners," Chest, vol. 139, no. 6,

pp. 1458-1462, 2011.

[57] T. J. Smith, "Occupational exposure and dose over time: Limitations of cumulative

exposure," American Journal of Industrial Medicine, vol. 21, pp. 35-51, 1992.

[58] M. H. Ross and J. Murray, "Occupational lung disease in mining," Occupational

Medicine, vol. 54, pp. 304-310, 2004.

[59] NIOSH, "NIOSH guide to the selection and use of particulate respirators certified

under 42 CFR 84, DHHS (NIOSH) Publication No. 96-101," U.S. Department

of Health and Human Services, Public Health Service, Centers for Disease

Control and Prevention, National Institute for Occupational Safety and Health,

Washington, DC, 1996.

[60] M. C. White, E. L. Baker, M. B. Larson and R. Wolford, "The role of personal beliefs

and social influences as determinants of respirator use among construction

painters," Scandinavian Journal of Work, Environment & Health, vol. 14, no.

4, pp. 239-245, 1988.

[61] L. Hongfei, M. L. Wang, N. Seixas, A. Ducatman and E. L. Petsonk, "Respiratory

protection: Associated factors and effectiveness of respirator use among

underground coal miners," American Journal of Industrial Medicine, vol. 42,

pp. 55-62, 2002.

[62] H. E. Harris, W. C. DeSieghardt, W. A. Burgess and P. C. Reist, "Respirator usage

and effectiveness in bituminous coal mining operations," American Industrial

Hygiene Association Journal, vol. 35, no. 3, pp. 159-164, 1972.

58

[63] G. Syamlal, B. Doney, K. M. Bang, M. Greskevitch, D. Groce and H. W. Ganocy,

"Medical fitness evaluation for respirator users: results of a national survey of

private sector employers," Journal of Occupational and Environmental

Medicine, vol. 49, no. 6, pp. 691-699, 2007.

[64] B. C. Doney, D. W. Groce, D. L. Campbell, M. F. Greskevich, W. A. Hoffman, P. J.

Middendorf, G. Syamlal and W. M. Bang, "A survey of private sector

respirator use in the United States: An overview of findings," Journal of

Occupational Environmental Hygiene, vol. 2, no. 5, pp. 267-276, 2005.

[65] W. M. Marine, D. Gurr and M. Jacobsen, "Clinically important respiratory effects of

dust exposure and smoking in British coal miners," American Review of

Respiratory Disease, vol. 137, no. 1, pp. 106-112, 1988.

[66] E. L. Petsonk, C. Rose and R. Cohen, "Coal mine dust lung disease -- New lessons

from an old exposure," American Journal of Critical Care Medicine, vol. 187,

no. 11, pp. 117-1185, 2013.

[67] I. Ates, H. S. Suzen, B. Yucesoy, I. O. Tekin and A. Karakaya, "Association of

cytokine gene polymorphisms in CWP and its severity in Turkish coal

workers," American Journal of Industrial Medicine, vol. 51, pp. 741-747,

2008.

[68] B. Yucesoy, V. J. Johnson, G. E. Kissling, K. Fluharty, M. L. Kashon, J. Slaven, D.

Germolee, V. Vallyathan and M. I. Luster, "Genetic susceptibility to

progressive massive fibrosis in coal miners," European Respiratory Journal,

vol. 31, pp. 1177-1182, 2008.

[69] R. Altin, R. F. Armuteu, L. Kart, A. Gurel, A. Savranlar and H. Özdemir,

59

"Antioxidant response at early stages and low grades of simple coal worker's

pneumoconiosis diagnosed by high resolution computed tomography,"

International Journal of Hygiene and Environmental Health, vol. 96, pp. 455-

462, 2004.

[70] W. R. L. James, "The relationship of tuberculosis to the development of massive

pneumokoniosis in coal workers," British Journal of Tuberculosis and

Diseases of the Chest, vol. 48, no. 2, pp. 89-96, 1954.

[71] C. M. Wiener, P. J. Nivatpumin, C. J. Brown, A. R. Hemnes and T. R. Harrison,

Harrison's principles of internal medicine: self-assessment and board review,

16th ed., New York: McGraw-Hill, Medical Publication Division, 2004.

[72] V. Castranova and V. Vallyathan, "Silicosis and Coal Workers' Pneumoconiosis,"

Environmental Health Perspectives, vol. 108, no. Supplement 4, pp. 675-684,

2000.

[73] H. R. Leavell and E. G. Clark, Preventive Medicine for the Doctor in His

Community, 3rd ed., New York: McGraw-Hill Book Company, 1965.

[74] P. S. Parobeck and R. A. Jankowski, "Assessment of the respirable dust levels in the

nation's underground and surface coal mining operations," American

Industrial Hygiene Association Journal, vol. 40, pp. 910-915, 1979.

[75] J. L. Weeks, "The fox guarding the chicken coop: Monitoring exposure to coal mine

dust, 1969-2000," American Journal of Public Health, vol. 93, no. 8, pp. 1236-

1244, 2003.

[76] A. L. Cochrane, "The attack rate of progressive massive fibrosis," British Journal of

Industrial Medicine, vol. 19, pp. 52-64, 1962.

60

[77] B. Prinz, R. Stolz, A. G. Ruhrkohle and F. R. G. Essen, "Effect of the measuring

strategy on the determination of the respirable dust concentration in the

breathable air at underground workplaces," in Proceedings of the VIIth

International Pneumoconioses Conference, Pittsburgh, PA and Cincinnati,

OH, 1990.

[78] Code of Federal Regulations, Washington, DC: U.S. Government Printing Office,

Office of the Federal Register.

[79] Federal Register, "75 Federal Register 64412," 19 October 2010. [Online]. Available:

http://www.msha.gov/REGS/FEDREG/PROPOSED/2010Prop/2010-

25249.pdf. [Accessed October 2013].

[80] OSHA, "Annotated TABLE Z-3 Mineral Dusts," 2012 January 2012. [Online].

Available: https://www.osha.gov/dsg/annotated-pels/tablez-3.html. [Accessed

October 2013].

[81] MSHA, "Review of the Program to Control Respirable Coal Mine Dust in the United

States -- Report of the Coal Mine Respirable Dust Task Group," U.S.

Department of Labor - Mine Safety and Health Administration, Washington,

DC, 1992.

[82] W. R. Reed, J. C. Volkwein and G. J. Joy, "A company-perspective cost analysis of

the personal dust monitor (PDM)," International Journal of Mining and

Mineral Engineering Research, vol. 12, no. 3, pp. 179-202, 2007.

[83] EIA, "Annual Coal Report, 2012, Table 29. Average Sales Price of Coal by State and

Underground Mining Method," 2012. [Online]. Available:

http://www.eia.gov/coal/annual/pdf/table29.pdf. [Accessed December 2013].

61

[84] R. Weissman, "Labor The Great Coal Dust Scam," Multinational Monitor, July 1991.

[85] Secretary of Labor v. Keystone Coal Mining Corp. 151 F.3d 1096, 1998.

[86] M. J. Nieuwenhuijsen, Exposure assessment in occupational and environmental

epidemiology, London: Oxford University Press, 2003.

[87] NORA Mining Sector Council, "National Mining Agenda: For Occupational Safety

and Health Research and Practice in the U.S. Mining Sector," NIOSH,

Washington, DC, 2013.

[88] National Academy of Sciences, "Part II: Evaluation of Strategic Research Areas, 8

Review of Respiratory Disease Prevention Research," in Mining Safety and

Health Research at NIOSH: Reviews of Research Programs of the National

Institute for Occupational Safety and Health, Washington, DC, The National

Academies Press, 2007.

[89] NIOSH OMSHR, "DVTSB Project Overview, FY 2014 (Internal Document),"

NIOSH OMSHR, Pittsburgh, PA, 2014.

[90] R. E. Glenn, "A critical review of the paper "Coal workers' pneumoconiosis in the

United States: Regional differences 40 years after implementation of the 1969

Federal Coal Mine Health and Safety Act" by Suryatha, E., Laney, A.S.,

Storey, E. et al.," 10 June 2011. [Online]. Available:

http://www.msha.gov/REGS/Comments/2010-25249/AB64-COMM-73-5.pdf.

[Accessed October 2013].

[91] A. S. Laney and M. D. Attfield, "Examination of potential sources of bias in the US

Coal Workers' Health Surveillance Program," American Journal of Public

Health, vol. 104, no. 1, pp. 165-170, 2014.

62

[92] Kentucky Department of Workers' Claims, "Kentucky Guidebook to Workers'

Compensation," Commonwealth of Kentucky, Frankfort, KY, 2011.

[93] C. Seltzer, "Health care by the ton," Health PAC (Policy Advisory Center), no.

November/December, pp. 1-8;25-33, 1977.

[94] B. E. Smith, "Digging our own graves: Coal miners and the struggle over black lung

disease," Thesis, Ph.D., Brandeis University, University Microfilms

International, Ann Arbor, MI, 1983.

[95] Department of Labor, "FY 2014 - Congressional Budget Justification - Black Lung

Disability Trust Fund," 2013. [Online]. Available:

http://www.dol.gov/dol/budget/2014/PDF/CBJ-2014-V2-08.pdf. [Accessed

October 2013].

[96] Department of Labor, "U.S. Department of Labor - Office of Workers' Compensation

Programs (OWCP) - Division of Coal Mine Workers' Compensation

(DCMWC) - Black Lung Program Statistics," 2013. [Online]. Available:

http://www.dol.gov/owcp/dcmwc/statistics/bls2012/DistributionOfClaimsBySt

ate2012.htm. [Accessed October 2013].

[97] Social Security Administration, "Annual Statistical Supplement, Black Lung

Benefits," 2012. [Online]. Available:

http://www.ssa.gov/policy/docs/statcomps/supplement/2012/blacklung.pdf.

[Accessed October 2013].

[98] T. L. Hungerford, "Federal Trust Funds and the Budget," Congressional Research

Service, Washington, DC, 2010.

[99] GAO, "Black Lung Benefits Program: Administrative and Structural Changes Could

63

Improve Miners' Ability to Pursue Claims (GAO-10-7)," US Government

Accountability Office, Washington, DC, 2009.

[100] C. Hamby, "Breathless and Burdened: Dying from black lung, buried by law and

medicine," Center for Public Integrity, Washington, DC, 2013.

[101] H. Berkes, "Johns Hopkins Halts, Reviews Black Lung Program," 4 November 2013.

[Online]. Available:

http://www.npr.org/blogs/thetwo-way/2013/11/04/243029509/johns-hopkins-

halts-reviews-black-lung-program. [Accessed February 2014].

[102] E. A. Spieler, "Can coal miners escape black lung? an analysis of the Coal Miner Job

Transfer Program and its implications for occupational medical removal

protection programs," School of Law Faculty Publications, p. 247, 1989.

[103] NIOSH, "NIOSH/DRDS/CWHSP Celebrates the 35th Anniversary of the Federal

Coal Mine Health and Safety Act," 2004. [Online]. Available:

http://www.cdc.gov/niosh/topics/surveillance/ords/CoalMineHealthSafetyAct3

5Years.html. [Accessed October 2013].

[104] G. Wagner and E. Spieler, "Is the US Chest X-Ray Surveillance Program Succeeding

in Controlling Lung Disease?," in Proceedings of the VII International

Conference on Pneumoconioses, Pittsburgh, PA, 1988.

[105] Mullins v. Beth-Elkhorn Coal Corp., 9 FMSHRC, 1987.

[106] NIOSH, Faces of Black Lung, DHHS (NIOSH) Publication No. 2008-131, NIOSH,

2008.

[107] R. H. Peters, C. Vaught, E. E. Hall and J. C. Volkwein, "Miners' view about Personal

Dust Monitors," Journal of the International Society for Respiratory

64

Protection, vol. 24, no. III-IV, pp. 74-92, 2007.

[108] National Mining Association, "CORESafety - Committed to Excellence in Mining

Safety," 2014. [Online]. Available: http://www.coresafety.org/. [Accessed

January 2014].

[109] G. J. Joy, J. F. Colinet and D. D. Landen, "Coal workers' pneumoconiosis disparity

between Australia and the United States," Mining Engineering, vol. 64, no. 7,

pp. 65-71, 2012.

[110] D. J. Curran, Dead Laws for Dead Men: The Politics of Federal Coal Mine Health

and Safety Legislation, Pittsburgh and London: University of Pittsburgh Press,

1993.

[111] NIOSH, "Work-Related Lung Disease Surveillance System (eWoRLD): Appendix |

International Classification of Diseases (ICD) Codes," 28 March 2013.

[Online]. Available:

http://www2a.cdc.gov/drds/WorldReportData/html/ICDCodes.asp. [Accessed

October 2013].

[112] J. L. Weeks, "From explosions to black lung: A history of efforts to control coal mine

dust," Occupational Medicine, vol. 8, no. 1, January-March, pp. 1-17, 1993.

[113] W. Marshall, "Cases of spurious melanosis of the lungs or of phthisis melatonica,"

Lancet, pp. 271-274, 1834.

[114] J. A. Merchant, G. Taylor and T. K. Hodous, Coal workers' pneumoconiosis and

exposure to other carbonaceous dusts, J. A. Merchant, Ed., Washington, DC:

US Department of Health and Human Services, 1986, pp. 329-400.

[115] A. Meiklejohn, "The origin of the term anthracosis," British Journal of Industrial

65

Medicine, vol. 16, no. 4, pp. 324-325, 1959.

[116] F. A. Zenker, Ueber Staubinhalationskrankhelten der lungen, Leipzig, 1866.

[117] R. L. Cowie, J. Murray and M. R. Becklake, "Pneumoconiosis and other mineral dust-

related dieases," in Murray and Nadel's Textbook of Respiratory Medicine, 5th

Edition, R. J. Mason, V. C. Broaddus, T. R. Martin and al., Eds., Philadelphia

PA, Saunders Elsevier, 2010.

[118] B. E. Smith, "Black lung: The social production of disease," International Journal of

Health Services, vol. 11, no. 3, pp. 343-359, 1981.

[119] Der Saarländische Rundfunk, "Das Grubenunglück Luisenthal: Vor 50 Jahren

(German)," 7 February 2012. [Online]. Available:

http://www.sr-online.de/sronline/sr3/uebersicht/sr_3_thema/beitraege/

artikel17550.html. [Accessed December 2013].

66