CURRENT INTELLIGENCE BULLETIN 64

Coal Mine Dust Exposures and 

Associated Health Outcomes

A Review of Information Published Since 1995

DEPARTMENT OF HEALTH AND HUMAN SERVICES

Centers for Disease Control and Prevention

National Institute for Occupational Safety and Health

Current Intelligence Bulletin 64

Coal Mine Dust Exposures and 

Associated Health Outcomes

DEPARTMENT OF HEALTH AND HUMAN SERVICES

Centers for Disease Control and Prevention

National Institute for Occupational Safety and Health

A Review of Information Published Since 1995
ii

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DHHS (NIOSH) Publication No. 2011–172

April 2011

Safer • Healthier • PeopleTM
iii

Foreword

Since its inception in 1970 the National Institute for Occupational Safety and Health 

(NIOSH) has extensively investigated and assessed coal miner morbidity and mortality. This history of research encompasses epidemiology; medical surveillance; 

laboratory-based toxicology, biochemistry, physiology, and pathology; exposure 

assessment; disease prevention approaches; and methods development. The experience gained in those activities, together with knowledge from external publications 

and reports, was brought together in 1995 in a major NIOSH review and report 

of recommendations, entitled Criteria for a Recommended Standard—Occupational 

Exposure to Respirable Coal Mine Dust. This document had the following major 

recommendations:

1. Exposures to respirable coal mine dust should be limited to 1 mg/m3 as a 

time-weighted average concentration for up to a 10 hour day during a 40 

hour work week;

2. Exposures to respirable crystalline silica should be limited to 0.05 mg/m3 as 

a time-weighted average concentration for up to a 10 hour day during a 40 

hour work week;

3. The periodic medical examination for coal miners should include spirometry;

4. Periodic medical examinations should include a standardized respiratory 

symptom questionnaire;

5. Surface coal miners should be added to and included in the periodic medical 

monitoring.

This Current Intelligence Bulletin (CIB) updates the information on coal mine dust 

exposures and associated health effects from 1995 to the present. A principal intent 

is to determine whether the 1995 recommendations remain valid in the light of the 

new findings, and whether they need to be updated or supplemented. The report 

does not deal with issues of sampling and analytical feasibility nor technical feasibility in achieving compliance.

John Howard, MD

Director, National Institute for

 Occupational Safety and Health

Centers for Disease Control and Prevention
iv

Executive Summary

Information relating to occupational pulmonary disease morbidity and mortality of 

coal miners available up to 1995 was reviewed in the NIOSH publication: Criteria 

for a Recommended Standard—Occupational Exposure to Respirable Coal Mine Dust, 

or Coal Criteria Document (CCD). This led to the following principal conclusions 

concerning health effects associated with coal mining:

1. Exposure to coal mine dust causes various pulmonary diseases, including 

coal workers’ pneumoconiosis (CWP) and chronic obstructive pulmonary 

disease (COPD). 

2. Coal miners are also exposed to crystalline silica dust, which causes silicosis, 

COPD, and other diseases.

3. These lung diseases can bring about impairment, disability and premature 

death. 

This Current Intelligence Bulletin updates the previously published review with respect to findings relevant to the health of U.S. coal miners published since 1995. The 

main conclusions are:

1. After a long period of declining CWP prevalence, recent surveillance data 

indicate that the prevalence is rising. 

2. Coal miners are developing severe CWP at relatively young ages (<50 years).

3. There is some indication that early development of CWP is being manifested 

as premature mortality. 

4. The above individuals would have been employed all of their working lives 

in environmental conditions mandated by the 1969 Coal Mine Health and 

Safety Act.

5. The increase in CWP occurrence appears to be concentrated in hot spots of 

disease mostly concentrated in the central Appalachian region of southern 

West Virginia, eastern Kentucky, and western Virginia.

6. The cause of this resurgence in disease is likely multifactorial. Possible explanations include excessive exposure due to increases in coal mine dust levels 

and duration of exposure (longer working hours), and increases in crystalline 

silica exposure (see below). As indicated by data on disease prevalence and 

severity, workers in smaller mines may be at special risk.

7. Given that the more productive seams of coal are being mined out, a transition by the industry to mining thinner coal seams and those with more rock 
v

intrusions is taking place and will likely accelerate in the future. Concomitant 

with this is the likelihood of increased potential for exposure to crystalline 

silica, and associated increased risk of silicosis, in coal mining.

The main conclusions drawn from review of the new information are:

1. While findings published since 1995 refine or add further to the understanding of the respiratory health effects of coal mine dust described in the NIOSH 

CCD, they do not contradict or critically modify the primary conclusions and 

associated recommendations given there. Rather, the new findings strengthen those conclusions and recommendations.

2. Overall, the evidence and logical basis for recommendations concerning 

prevention of occupational respiratory disease among coal miners remains 

essentially unaffected by the newer findings that have emerged since publication of the CCD. 

In summary, as recommended by the CCD, every effort needs to be made to reduce 

exposure to both coal mine dust and to crystalline silica dust. As also recommended 

in the CCD, the latter task requires establishing a separate compliance standard in 

order to provide an effective limit to exposure to crystalline silica dust.

vii

Contents

Foreword. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iii

Executive Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iv

List of Figures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . viii

List of Tables. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . x

Abbreviations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xi

Glossary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xii

Acknowledgments. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiv

1 Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

2 Coal Workers’ Pneumoconiosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

2.1 Surveillance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

2.2 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

2.3 Mortality. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

2.4 Toxicology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

2.5 Risk analysis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

3 Other Respiratory Disease Outcomes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

3.1 Risk Analysis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

4 Cancer Outcomes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

5 Dust Exposure Levels, Control, And Compliance. . . . . . . . . . . . . . . . . . . . . . . . . 27

5.1 Dust Exposure Levels. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

5.2 Dust Exposure Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

5.3 Compliance Policy and Procedures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

6 Surface Coal Mining. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

7 Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

8 References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33
viii

List of Figures

Figure 1. Prevalence of CWP category 1 or greater from the NIOSH Coal Workers’ X-ray Program from 1970–1995, by tenure in coal mining.

Figure 2. Trend in reported dust concentrations for continuous miner operators, 

1968–87.

Figure 3. Probability that an individual starting with no pneumoconiosis (category 0/0) will be classified as 2/1 or greater after 35 years of exposure to 

various concentrations of coal mine dust.

Figure 4. Predicted prevalence of PMF among British coal miners after a 35-year 

working lifetime by mean concentration of respirable coal mine dust.

Figure 5. Prevalence of simple CWP category 1 or greater among U.S. coal miners 

by estimated cumulative dust exposure and coal rank.

Figure 6. Prercentage of evaluated miners with rapidly progressive coal workers’ 

pneumoconiosis by county.

Figure 7. Percentage of miners in the NIOSH Coal Workers’ X-ray Surveillance 

Program with coal workers’ pneumoconiosis (category 1 or greater) 

from 1970–2009, by tenure in coal mining.

Figure 8. Percentage of miners examined in the NIOSH Coal Workers’ X-ray Surveillance Program with progressive massive fibrosis (PMF) from 1970–

2009, by tenure in mining.

Figure 9. Observed and predicted prevalences (%) of CWP category 1 or greater 

by age group and MSHA District.

Figure 10. Hours worked per underground coal miner, 1978–2008.

Figure 11. Tons produced per hour worked at underground coal mines, 1978–2008.

Figure 12. Respirable coal mine dust: Geometric mean exposures by type of mine 

(UG=underground, SU=surface), MSHA inspector (INSP) and mine 

operator (OPER) samples.

Figure 13. Ratio of special inspection sample values to preceding operator compliance sample values by mine size.

Figure 14. Age-adjusted death rates (per million) for decedents age ≥25 years with 

coal workers’ pneumoconiosis as the underlying cause of death—United 

States, 1968–2006.
ix

Figure 15. Years of potential life lost (YPLL) before age 65 and mean YPLL per decedent for decedents aged ≥25 years with coal workers’ pneumoconiosis 

as the underlying cause of death—United States, 1968–2006.

Figure 16. Risks at age 58–60 after 35–40 working years of: PMF; category 2 or 

greater; 993 ml deficit of FEV1 in nonsmokers; 993 ml deficit of FEV1 in 

smokers.

Figure 17. Risks for category 2 silicosis in relation to respirable silica concentration 

(<2 mg/m3) averaged over 15 years.

Figure 18. Respirable quartz dust: Geometric mean exposures by type of coal mine.
x

List of Tables

Table 1. Predicted prevalence of simple CWP and PMF among U.S. or British 

coal miners at age 58 following exposure to respirable coal mine dust 

over a 40-year working lifetime. 

Table 2. Predicted prevalence of decreased lung function among U.S. or British 

coal miners at age 58 following exposure to respirable coal mine dust 

over a 40-year working lifetime. 

Table 3. Excess (exposure-attributable) prevalence of simple CWP or PMF 

among U.S. coal miners at age 65 following exposure to respirable coal 

mine dust over a 45-year working lifetime. 

Table 4. Excess (exposure-attributable) prevalence of decreased lung function 

among U.S. coal miners at age 65 following exposure to respirable coal 

mine dust over a 45-year working lifetime.
xi

Abbreviations

CAO chronic airway obstruction

CCD coal criteria document, formally NIOSH Criteria for a Recommended 

Standard—Occupational Exposure to Respirable Coal Mine Dust

COPD chronic obstructive pulmonary disease 

CWP coal workers’ pneumoconiosis

CWXSP Coal Workers’ X-ray Surveillance Program

FEV1 forced expiratory volume in 1 second

ILO International Labour Office

mg/m3 milligrams per cubic meter

MSHA Mine Safety and Health Administration

NIOSH National Institute for Occupational Safety and Health

PAH polycyclic aromatic hydrocarbons

PDM personal continuous dust monitor

PMF progressive massive fibrosis

REL recommended exposure limit

YPLL years of potential life lost
xii

Glossary

Aerodynamic diameter: The diameter of a sphere with a density of 1 g/cm3 and with 

the same stopping time as the particle. Particles of a given aerodynamic diameter move 

within the air spaces of the respiratory system identically, regardless of density or shape.

Chronic obstructive pulmonary disease (COPD): Includes chronic bronchitis (inflammation of the lung airways associated with cough and phlegm production), 

impaired lung function, and emphysema (destruction of the air spaces where gas 

transfer occurs). COPD is characterized by irreversible (although sometimes variable) obstruction of lung airways, and should be considered in any patient who has 

dyspnea, chronic cough or sputum, and/or a history of exposure to risk factors for 

COPD. The diagnosis should be confirmed by spirometry.

Coal rank: A classification of coal based on fixed carbon, volatile matter, and heating value of the coal. Coal rank indicates the progressive geological alteration (coalification) from lignite to anthracite.

Coal workers’ pneumoconiosis (CWP): A chronic dust disease of the lung arising 

from employment in a coal mine. In workers who are or have been exposed to coal 

mine dust, diagnosis is based on the radiographic classification of the size, shape, 

profusion, and extent of parenchymal opacities.

Crystalline silica: Silicon dioxide (SiO2). “Crystalline” refers to the orientation of 

SiO2 molecules in a fixed pattern as opposed to a nonperiodic, random molecular 

arrangement defined as amorphous. The three most common crystalline forms of 

free silica encountered in general industry are quartz, tridymite, and cristobalite. 

The predominant form is quartz.

Excess (exposure-attributable) prevalence: The prevalence (cases/population at 

risk) attributable to workplace dust exposure (in the case of CWP, the prevalence 

adjusted for radiographic appearances associated with lung aging).

International Labour Office (ILO) classification system: A standardized method for 

assessing abnormalities related to the pneumoconioses based substantially on comparison of test with reference radiographs. In the system there are 4 categories of simple 

pneumoconiosis (categories 0, 1, 2, and 3), with 0 implying no definite abnormality.

Progressive massive fibrosis: Coal workers’ complicated pneumoconiosis. Diagnosis is based on determination of the presence of large opacities (1 cm or larger) using 

radiography or the finding of specific lung pathology on biopsy or autopsy.
xiii

Quartz: Crystalline silicon dioxide (SiO2) not chemically combined with other substances and having a distinctive physical structure.

Respirable coal mine dust: That portion of airborne dust in coal mines that is capable of entering the gas-exchange regions of the lungs if inhaled: by convention, 

a particle-size-selective fraction of the total airborne dust; includes particles with 

aerodynamic diameters less than approximately 10 μm.
xiv

Acknowledgments

Michael Attfield was the primary author of this document, which was prepared in 

the Division of Respiratory Disease Studies, NIOSH, under the direction of Dr. David Weissman. He acknowledges the following assistance in the preparation of the 

report:

Division of Respiratory Disease Studies (DRDS)

Janet Hale, Eva Suarthana, Mei Lin Wang

Health Effects Laboratory Division (HELD)

Vincent Castranova, Kimberly Clough Thomas

This Current Intelligence Bulletin has undergone substantial internal and external 

scientific peer review with subsequent revision. A draft version of the document was 

published on the NIOSH website for public comment for 60 days, with notification 

of its availability via the Federal Register. All input, both internal and external, has 

been considered, addressed, and responded to in preparation of this final version. 

Internal NIOSH reviewers who provided critical feedback to the preparation 

of the document

Eileen Kuempel, Education and Information Division (EID). Ed Thimons, Office 

of Mine Safety and Health Research (OMSHR), Robert Castellan (DRDS), Ainsley 

Weston (DRDS), Eileen Storey (DRDS).

External Expert Peer Review Panel

NIOSH expresses appreciation to the following independent, external reviewers for 

providing insights and comments that contributed to the development of this document and enhanced the final version:

Robert Cohen, M.D., F.C.C.P.

Cook County Health and 

 Hospitals System

Chicago, IL

Dennis O’Dell

United Mine Workers of America

Washington, DC

Joseph Lamonica

Bituminous Coal Operators

 Association

Washington, DC

Cecile Rose, M.D.

National Jewish Health

Denver, CO
1

1 Introduction

undertaken primarily in the U.S., the United 

Kingdom, and (West) Germany, with supporting information coming from studies in other 

European countries and Australia.

The available information was thoroughly summarized in the CCD. It showed that, in 1995, 

CWP was in decline in the U.S., with downward 

trends in prevalence in all tenure groups (Figure 

4–2 of the CCD (1), included here as Figure 1). 

This decline was consistent with reductions in 

coal mine dust exposure mandated by the 1969 

Coal Mine Health and Safety Act (1969 Coal 

Mine Act) (CCD Figure 4–1 (1); Figure 2). Despite this decline in disease levels, NIOSH concluded from review of the surveillance data and 

quantitative risk estimates based on the epidemiologic studies that the current dust exposure 

regulations for U.S. coal mines were not sufficiently protective. Consequently, it proposed 

lower dust limits for coal mines, enhanced medical surveillance, and other requirements. 

The publication of the NIOSH Criteria for a Recommended Standard—Occupational Exposure 

to Respirable Coal Mine Dust or Coal Criteria 

Document (CCD) in 1995 (1) followed a long 

period of extensive research activity focused 

on exposure to coal mine dust and its health 

effects in coal miners. From this research, 

substantial information had emerged about 

the extent and severity of respiratory disease 

caused by coal mine dust, its quantitative relationship with dust exposure, its pathology and 

toxicology, environmental patterns of relevant 

exposures, and methodologies for assessing 

these variables. In particular, the findings demonstrated that not only was there a considerable burden of coal workers’ pneumoconiosis 

(CWP) in the U.S. and other countries, but that 

underground coal miners were vulnerable to 

other lung diseases, notably chronic obstructive pulmonary disease (COPD). The evidence 

came from extensive and well-planned epidemiologic and laboratory-based investigations 

Figure 1. Prevalence of CWP category 1 or greater from the NIOSH Coal Workers’ X-ray Program 

from 1970–1995, by tenure in coal mining. (Figure 4–2 of the CCD (1)).
2 NIOSH CIB 64 • Coal Mine Dust Exposures

The CCD noted that the current U.S. federal 

dust limit for underground coal mines dated 

back to the 1969 Coal Mine Act, which mandated a compliance permissible exposure limit 

of 2 milligrams per cubic meter (mg/m3) of respirable coal mine dust. This limit was derived 

from British research, which provided the only 

quantitative exposure-response relationship 

available at that time. This exposure-response 

curve (CCD Figure 7–2 (1); Figure 3) predicted 

that no cases of CWP as severe as category 2 on 

the International Labour Office (ILO) classification system (3) would develop among miners who worked 35 years at 2 mg/m3

. Similarly 

at that time, the current information indicated 

that the disabling form of CWP, progressive 

massive fibrosis (PMF), was very unlikely to 

develop from less severe ILO categories (e.g., 

category 1 CWP). Therefore, adoption of the 

2 mg/m3 limit was believed, at that time, to be 

protective against the risk of disability and premature mortality that accompanies PMF.

Subsequent scientific findings, emerging between 1969 and 1995, disproved some of the 

assumptions inherent in the adoption of the 

2 mg/m3 standard. Firstly, the assumption that 

miners with CWP less severe than category 2 

were at minimal risk of PMF was found to be 

incorrect. Moreover, additional findings from 

the British data (CCD Figure 7–6 and Table 

4–6 (1); Figure 4 and Table 1), together with 

new results on U.S. underground coal miners 

from research undertaken by NIOSH (CCD 

Figure 7–4 and Table 4–6 (1); Figure 5 and 

Table 1) showed that there was no threshold at 

2 mg/m3 as had been indicated by the original 

British study (CCD Figure 7–2 (1); Figure 3). 

Furthermore, the CCD reviewed findings on 

other lung diseases and their relationship with 

coal mine dust exposure. It concluded that coal 

miners were at additional risk of developing 

ventilatory function deficits, respiratory symptoms, and emphysema in addition to CWP 

(CCD Table 4–7 (1); Table 2). (Note that the 

Figure 2. Trend in reported dust concentrations for continuous miner operators, 1968–87. [Figure 

4–1 of the CCD (1)] (Source: Attfield and Wagner (2)).
NIOSH CIB 64 • Coal Mine Dust Exposures 3

Figure 3. Probability that an individual starting with no pneumoconiosis (category 0/0) will be 

classified as 2/1 or greater after 35 years of exposure to various concentrations of coal mine dust. 

[Figure 7–2 of the CCD (1)] (Source: Jacobsen et al. (4)).

Figure 4. Predicted prevalence of PMF among British coal miners after a 35-year working lifetime 

by mean concentration of respirable coal mine dust. [Figure 7–6 of the CCD (1)](Source: Hurley 

and Maclaren (5)).
4 NIOSH CIB 64 • Coal Mine Dust Exposures

Table 1. Predicted prevalence of simple CWP and PMF among U.S. or British coal miners at 

age 58 followingT exposure to respirable coal mine dust over a 40-year working lifetime. 

(Table 4–6 of the CCD(1))

*Attfield and Seixas (6) define the coal rank groups as follows: 1- high-rank bituminous (89–90% carbon)—central Pennsylvania and 

southern West Virginia; 2-medium/low-rank bituminous (80–87% carbon)—western Pennsylvania, northern and southwestern West 

Virginia, eastern Ohio, eastern Kentucky, western Virginia and Alabama; 3- low-rank—western Kentucky, Illinois, Utah, and Colorado. †

Ninety-five percent confidence intervals, where available, are in parentheses under the point estimates for prevalence (cases/ 1000).

‡

In Attfield and Morring (7), the predicted prevalences for CWP category 1 or greater and category 2 or greater did not include PMF (correction from CCD original). §

Attfield and Morring (7) define the coal rank groups as follows: 1- anthracite - two mines in eastern Pennsylvania (~93% carbon); 2- medium/low-volatile bituminous (89–90% carbon)—three mines in central Pennsylvania and three in southeastern West Virginia; 3- highvolatile “A” bituminous (80–87% carbon)—16 mines in western Pennsylvania, north and southwestern West Virginia, eastern Ohio, 

eastern Kentucky and Illinois.

Study and coal rank

Mean concentration of 

respirable CMD (mg/m3)

Predicted prevalence (cases/1,000)

CWP≥1 CWP≥2 CWP≥3

Attfield and Seixas (6):*

High-rank bituminous 2.0 253 89 51

(204–308)† (60–130) (30–85)

1.0 116 29 16

(88–150) (16–51) (7–36)

Medium/low-rank bituminous 2.0 144 31 14

(117–176) (20–49) (7–27)

1.0 84 17 9

(64–110) (9–30) (4–19)

Attfield and Morring (7):‡

Anthracite 2.0 316 142 89

(278–356) (118–172) (69–113)

1.0 128 46 34

(108–152) (35–60) (24–48)

High-rank bituminous 2.0 282 115 65

 (89% carbon) (250–317) (94–141) (49–85)

1.0 119 41 29

(100–142) (31–54) (20–41)

Medium/low rank bituminous 2.0 121 40 22

 (83% carbon) (108–136) (33–49) (17–29)

1.0 74 24 17

(62–89) (18–31) (12–24)

Medium/low-rank bituminous 2.0 89 28 15§

 (Midwest) (73–108) (20–39) (9–26)

1.0 63 20 14§

(52–77) (14–27) (9–21)

Medium/low rank bituminous 2.0 67 15 13§

 (West) (52–86) (8–26) (7–24)

1.0 55 14 12§

(44–68) (10–21) (8–20)

Hurley and Maclaren

High-rank bituminous 2.0 89 29 18

 (89% carbon)

1.0 40 12 7

Medium/low-rank bituminous 2.0 65 16 7

 (83% carbon)

1.0 28 7 3
NIOSH CIB 64 • Coal Mine Dust Exposures 5

results provided here are selected to illustrate 

the main CCD conclusions. For a full understanding of the complete body of knowledge, 

please see the CCD (1).) 

On the basis of the updated body of evidence 

on the adverse health effects and an evaluation of the technological feasibility of reducing dust exposures, NIOSH recommended 

that the federal coal mine dust limit be reduced to 1 mg/m3

. Critical to this decision 

were computed excess (exposure-attributable) 

prevalences of CWP derived from two studies of U.S. coal miners undertaken by NIOSH 

(CCD Table 7–2 (1); Table 3). Predictions were 

derived from each study for a working lifetime 

(i.e., 45 years) exposure at 2 mg/m3 and 1 mg/

m3. Another source of information critical to 

the recommendations was information on predicted excess lung function decrements for a 

lifetime’s exposure to 1 mg/m3 and 2 mg/m3

respectively (CCD Table 7–3 (1); Table 4). Details of the rationale for, and development of, 

the risk analyses employed in the CCD were 

subsequently published separately (8). NIOSH 

also evaluated information from other epidemiologic studies in coming to its recommendations in the CCD. However, because no other studies had quantitative exposure-response 

information, apart from strengthening the 

Figure 5. Prevalence of simple CWP category 1 or greater among U.S. coal miners by estimated 

cumulative coal mine dust exposure and coal rank. [Figure 7–4 of the CCD (1)](Source: Attfield 

and Seixas (6)).
6 NIOSH CIB 64 • Coal Mine Dust Exposures

In addition to recommending a reduction in 

the exposure limit for coal mine dust, NIOSH 

also recommended a change in the exposure 

limit for crystalline silica dust and the method 

by which it is enforced. Currently, silica levels 

are intended to be controlled by a reduction in 

the level of coal mine dust commensurate with 

the proportion of the dust that is silica. NIOSH 

proposed a separate limit for respirable crystalline silica in order to more effectively monitor 

case for more stringent regulation, these additional study results did not provide any numerical basis for standard setting. For simplicity, NIOSH recommended one exposure limit 

for the nation rather than different limits by 

coal rank, based on technological feasibility of 

reducing exposures, even though CWP prevalence has been shown to vary according to the 

rank of the coal in studies of miners in the U.S. 

and other countries. 

Table 2. Predicted prevalence of decreased lung function* among U.S. or British coal miners 

at age 58 following exposure to respirable coal mine dust over a 40-year working lifetime. 

(Table 4–7 of the CCD (1))

*Decreasing lung function is defined as FEV1 <80% of predicted normal values. Clinically important deficits are FEV1 

<80%, which approximately equals the lower limit of normal (LLN), or the fifth percentile (9, 10); and FEV1 <65%, 

which has been associated with severe exertional dyspnea (11, 12). †

Attfield and Hodous (13) define the following coal rank regions: East—anthracite (eastern Pennsylvania) and bituminous (central Pennsylvania, northern Appalachia [Ohio, northern West Virginia, western Pennsylvania], southern 

Appalachia [southern West Virginia, eastern Kentucky, western Virginia]), Midwest (Illinois, western Kentucky), 

and South (Alabama). ‡

Conversion from gh/m3 to mg-yr/m3; assumed 1,920 hr/yr for U.S. miners.

Predicted prevalence (cases/1,000)

Study and region†

Mean concentration of 

respirable coal mine 

dust (mg/m3)

Lung function 

decrement

(% FEV1)

Never

smokers Smokers

Attfield and Hodous (8)

East 2.0 <80 141 369

<65 22 102

1.0 <80 123 336

<65 18 87

West 2.0 <80 125 340

<65 16 80

1.0 <80 108 309

<65 13 68

Marine et al. (9):

2.0 <80 153 372

<65 63 173

1.0 <80 125 314

<65 52 159
NIOSH CIB 64 • Coal Mine Dust Exposures 7

Table 3. Excess (exposure-attributable) prevalence of simple CWP or PMF among U.S. coal 

miners at age 65 following exposure to respirable coal mine dust over a 45-year working 

lifetime. (Table 7–2 of the CCD (1))

*Attfield and Seixas (6) define the coal rank groups as follows: 1- high-rank bituminous (89–90% carbon)—central 

Pennsylvania and southern West Virginia; 2- medium/low-rank bituminous (80–87% carbon)—western Pennsylvania, northern and southwestern West Virginia, eastern Ohio, eastern Kentucky, western Virginia and Alabama; 

3- low-rank—western Kentucky, Illinois, Utah and Colorado. †

Attfield and Morring (7) define the coal rank groups as follows: 1- anthracite - two mines in eastern Pennsylvania 

(~93% carbon); 2- medium/low-volatile bituminous (89–90% carbon)—three mines in central Pennsylvania and 

three in southeastern West Virginia; 3- high-volatile “A” bituminous (80–87% carbon)—16 mines in western Pennsylvania, north and southwestern West Virginia, eastern Ohio, eastern Kentucky and Illinois.

Study and coal rank Disease category

Cases/1,000 at various mean dust concentrations

0.5 mg/m3 1.0 mg/m3 2.0 mg/m3

Attfield and Seixas (6):*

High-rank CWP ≥ 1 48 119 341

bituminous CWP ≥ 2 20 58 230

PMF 13 36 155

Medium/low-rank CWP ≥ 1 27 63 165

bituminous CWP ≥ 2 9 22 65

PMF 4 10 29

Attfield and Morring (7):†

Anthracite CWP ≥ 1 45 120 380

CWP ≥ 2 17 51 212

PMF 17 46 167

High-rank CWP ≥ 1 41 108 338

bituminous CWP ≥ 2 15 43 168

(89% carbon) PMF 13 34 114

Medium/low-rank CWP ≥ 1 18 42 111

bituminous CWP ≥ 2 6 15 42

(83% carbon) PMF 4 9 21

Medium/low-rank CWP ≥ 1 12 26 64

bituminous CWP ≥ 2 4 9 22

(Midwest) PMF 1 3 6

Medium/low-rank CWP ≥ 1 7 14 32

bituminous CWP ≥ 2 <1 <1 1

(West) PMF <1 <1 1
8 NIOSH CIB 64 • Coal Mine Dust Exposures

Table 4. Excess (exposure-attributable) prevalence of decreased lung function* among U.S. 

coal miners at age 65 following exposure to respirable coal mine dust over a 45-year working lifetime. (Table 7–3 of the CCD (1))

*Decreasing lung function is defined as FEV1 <80% of predicted normal values. Clinically important deficits are FEV1

<80%, which approximately equals the lower limit of normal (LLN), or the fifth percentile (9, 10); and FEV1 <65%, 

which has been associated with severe exertional dyspnea (11, 12). †

Attfield and Hodous (8) define the following coal rank regions: East—anthracite (eastern Pennsylvania) and bituminous (central Pennsylvania, northern Appalachia [Ohio, northern West Virginia, western Pennsylvania], southern 

Appalachia [southern West Virginia, eastern Kentucky, western Virginia]), Midwest (Illinois, western Kentucky), 

and South (Alabama). ‡

Coal rank was not provided in Seixas et al. (14) However, miners were included from bituminous coal ranks and regions across the United States, as described in Attfield and Seixas (6): 1. High-rank bituminous (89%–90% carbon): 

central Pennsylvania and southeaster West Virginia; 2. Medium/low-rank bituminous (80%–87% carbon): mediumrank—western Pennsylvania, northern and southwestern West Virginia, eastern Ohio, eastern Kentucky, western 

Virginia, and Alabama; low-rank—western Kentucky, Illinois, Utah, and Colorado.

Cases/1,000 at various mean

dust concentrations

Study and region

Lung function 

decrement Smoking status 0.5 mg/m3 1.0 mg/m3 2.0 mg/m3

Attfield and Hodus (8):†

East <80% FEV1 Never smoked 10 21 44

Smoker 12 24 51

West <80% FEV1 Never smoked 9 19 40

Smoker 11 23 48

East <65% FEV1 Never smoked 2 5 12

Smoker 4 8 19

West <65% FEV1 Never smoked 2 4 9

Smoker 3 7 15

Seixas et al. (14): <80% FEV1 Never smoked 60 134 315

Smoker 68 149 338

<65% FEV1 Never smoked 18 45 139

Smoker 27 67 188
NIOSH CIB 64 • Coal Mine Dust Exposures 9

and control exposures. The NIOSH recommendations for coal mine dust and crystalline silica 

dust were explicitly intended for both underground and surface coal operations. In addition, NIOSH recommended enhancing worker 

medical monitoring, and extending it to surface 

coal mine workers. An independent advisory 

committee, which was convened by MSHA in 

1996 in response to the NIOSH CCD, affirmed 

each of the recommendations in the CCD (15). 

The following material comprises a summary 

of results from reports that have been published since 1995 on CWP, other respiratory 

diseases, cancer outcomes, and overall mortality. In addition, new information summarized 

from the current NIOSH medical monitoring 

program for coal miners is included. There are 

also sections on aspects relating to dust levels, 

control, and compliance, and on surface coal 

mining. 

NIOSH CIB 64 • Coal Mine Dust Exposures 11

2 Coal Workers’ Pneumoconiosis

other reports included: 5) longer hours being 

worked by today’s coal miners; 6) excessive exposure to crystalline silica, perhaps associated 

with the mining of thinner seams of coal; and 

7) lack of resources for dust control and miner/operator education, particularly in smaller 

mines (19–21). 

To gain a better understanding of the extent of 

the problem, NIOSH undertook a systematic 

analysis of rapidly progressive CWP (22). Statistics were derived based on each miner’s radiographic steps of progression of CWP using 

the standard ILO categorical scores standardized to a five-year interval. These data were 

summarized by county and then plotted to 

reveal ‘hot spots’ of rapid disease progression 

(Figure 6; from Antao et al, 2005 (22)). These 

tended to be located on the eastern edge of the 

Appalachian coal field but were particularly 

concentrated in the southern West Virginia 

(WV)/western VA/eastern KY tri-state region 

(central Appalachian region). 

In response to these observations, NIOSH undertook a series of field surveys in the hot spot 

regions in an attempt to enhance the quality 

of data (i.e., improve participation). The field 

surveys were undertaken as part of the Coal 

Workers’ X-ray Surveillance Program (CWXSP) administered by NIOSH, as mandated by 

the 1969 Coal Mine Act. The targeted surveys 

comprised an “Enhanced Program” to complement the regular CWXSP program. Those 

findings are included in an overall tabulation 

that can be found in the NIOSH 2007 Workrelated Lung Disease (WoRLD) Surveillance 

Report (disseminated in hard copy (23) and 

2.1 Surveillance

Over time since 1995 it has become increasingly apparent that the observed prevalence 

of CWP in U.S. underground coal miners examined in the Coal Miners’ X-ray Surveillance 

Program (CWXSP) was no longer declining 

as it had from 1969–1995, but had begun increasing. This situation was first noticed in a 

2003 CDC/NIOSH report (16). This report 

also drew attention to the fact that CWP was 

developing in underground coal miners who 

had spent all of their working life in a working 

environment where the dust conditions should 

have been as mandated by the 1969 Coal Mine 

Act. Based on findings that showed higher 

CWP prevalences in certain worker groups, 

the publication raised concerns about possible 

excessive dust exposures in certain states, at 

smaller mines, and by some surface and contract miners. 

Reports in 2006 and 2007 called attention to 

advanced pneumoconiosis in working underground miners in Kentucky (KY) and Virginia 

(VA) (17, 18); as with the prior report (2003), 

most of the affected miners had started work 

after 1969 yet had still developed severe CWP. 

Possible reasons put forth as explanations for 

the findings were: 1) inadequacies in the mandated coal mine dust regulations; 2) failure 

to comply with or adequately enforce those 

regulations; 3) lack of disease prevention innovations to accommodate changes in mining practices (e.g., thin-seam mining); and 4) 

missed opportunities by miners to be screened 

for early disease and take action to reduce 

dust exposures. Further explanations, noted in 
12 NIOSH CIB 64 • Coal Mine Dust Exposures

on the NIOSH internet site (24). These results 

showed that the prevalence of CWP appeared 

to have stopped declining around 1995–1999, 

and has risen since then. The trend reversal 

appears most apparent in the longer-tenured 

miners. Virtually that entire group had spent 

their whole working life in dust conditions 

mandated by the 1969 Coal Mine Act. An updated (unpublished) version of this graphic, 

taking the data up to 2009, shows the increased 

CWP prevalence observed over the past decade (Figure 7). 

The upward trend visible in Figure 7 for all 

pneumoconiosis cases (category 1+) is even 

more evident for PMF (Figure 8). Of particular 

concern are the prevalence values for the last 

three five-year periods (1995–2009) for miners with <25 years tenure, which are well above 

those observed in the early 1990s. In 2005–2009 

alone, 69 coal miners examined in the CWXSP 

were determined to have PMF. Of these, 11 had 

less than 25 years total tenure in coal mining, 

and the majority (56, or 81%) were working in 

the central Appalachian region. 

Since the data from 2005 in Figures 7 and 8 

were derived, in part, from the special NIOSH 

surveys targeted at hot spot areas, there could 

be the concern that the recent CWXSP findings may be upwardly biased, with the implication that the apparent rise in prevalence may 

be an artifact. However, overall prevalences 

for 2005–2009 for the Enhanced and regular 

programs, derived from state-specific prevalences weighted by the participation rates for 

the whole program from the different states 

gives rise to figures of 3.2% prevalence for 

data from the targeted surveys (Enhanced program) compared to 3.1% for data from the regular program. There is therefore no indication 

whatsoever of any major bias. Moreover, it is 

Figure 6. Percentage of evaluated miners with rapidly progressive coal workers’ pneumoconiosis by 

county (not shown are counties with fewer than five miners evaluated). (Source: Antao et al. (22)).
NIOSH CIB 64 • Coal Mine Dust Exposures 13

clear from Figures 7 and 8 that the upswing in 

prevalence of CWP was underway before the 

targeted surveys began in 2005. 

The finding of severe CWP in the CWXSP was 

confirmed among West Virginia coal miners 

with a report of 138 compensated cases of PMF 

from 2000–2009 (25). These miners had worked 

virtually all of their lives under post-1969 Coal 

Mine Act conditions, and had developed PMF 

at age 52.6 years on average. Of the 138, 21 had 

died by publication date. 

A number of reports of surveillance information from other countries have emerged since 

1995 (26–31). Although mining conditions 

differ in these other countries, these studies are 

supportive of the findings in U.S. coal miners. 

Figure 7. Percentage of miners examined with CWP category 1 or greater from the NIOSH Coal 

Workers’ X-ray Program from 1970–2009, by tenure in coal mining. (Source: NIOSH CWXSP data).

Figure 8. Percentage of miners examined with PMF from the NIOSH Coal Workers’ X-ray Program from 1970–2009, by tenure in coal mining. (Source: NIOSH CWXSP data).
14 NIOSH CIB 64 • Coal Mine Dust Exposures

2.2 Epidemiology

The CWXSP finding of increased prevalence 

of CWP has prompted a series of analyses by 

NIOSH aimed at identifying factors that might 

be causing the increase. In an analysis undertaken as part of this series (32), predicted risk 

of CWP was derived for each individual who 

participated in the CWXSP from 2005–2009 

using published exposure-response models 

(7). The models were coal-rank specific, and 

used both age and cumulative coal mine dust 

exposure as predictors. The resulting individual risks (lying between 0 and 1) were then 

summed over subsets of the data and compared with the observed prevalences. (Further 

models, published later, were also available, but 

the early relationships were preferred because 

they were based on greater numbers of observations and had more specific adjustment 

for coal rank. The later predicted prevalences 

were somewhat higher than those presented 

here.) The results tabulated by MSHA region 

and age are shown here in Figure 9. It is clear 

that CWP prevalence is less than expected 

in some regions (observed≤predicted) but 

substantially greater than expected in others 

Figure 9. Observed and predicted prevalences (%) of CWP category 1 or greater by age group and 

MSHA District. (Source: Data from the NIOSH CWXSP for 1995–2009. Charts based on data provided in Suarthana et al (32).)
NIOSH CIB 64 • Coal Mine Dust Exposures 15

(observed>predicted). That is, in the northern Appalachian region and the mid-west and 

western coal fields the observed prevalences 

are generally below those predicted in all age 

groups. However, in the southern WV, eastern 

and central KY, Tennessee, and VA MSHA regions the observed prevalences are 2–4 times 

greater than predicted from cumulative coal 

mine dust exposure and age. Clearly, some factor or factors must be acting differently across 

the regions to cause this regional pattern. 

At least three environmental factors impact 

the central Appalachian region in this respect. 

These are: thin seams, small mines, and, for 

VA, high coal rank. The mining of thin coal 

seams, which often involves the deliberate cutting and extraction of substantial amounts of 

(often siliceous) rock overlying or underlying 

the coal seam, is particularly prevalent in Appalachia (33). NIOSH has been investigating 

the health implications of possible excessive 

crystalline silica exposure arising from the 

cutting of the rock adjacent to the coal seams 

(34). This analysis used the presence of r-type 

pneumoconiotic opacities on the chest X-ray 

as an indicator of crystalline silica exposure. 

This type of opacity is a radiographic manifestation of nodules in the lung having a typology 

often associated with excessive exposure to silica dust. An increase in the prevalence of such 

opacities could then well indicate that miners 

are more frequently being exposed to crystalline silica dust, or are experiencing exposure to 

higher levels of silica dust. Increased exposure 

to crystalline silica dust may well be arising 

from industry trends, whereby there is greater 

focus on mining thinner seams of coal as the 

more productive thicker seams are mined out. 

The findings from this study indicated that 

the proportion of radiographs showing r-type 

opacities increased during the 1990s, and 

particularly after 1999, in KY, VA, and WV, 

compared to the 1980s. They could potentially 

be explained by an increase in the frequency 

and/or intensity of silica exposure among underground coal miners. This hypothesis was 

confirmed by evidence from dust sampling in 

mines in that region indicating that excessive 

silica exposures are occurring (35). In the CCD, 

NIOSH not only recommended that compliance procedures for crystalline silica be made 

more effective, but that the exposure limit be 

reduced. In the light of these epidemiological 

findings (34), therefore, this recommendation 

remains appropriate and even more urgent. A 

report on British coal miners also associated 

an increase in CWP prevalence with rock cutting (36). 

In another NIOSH analysis (19) trends in CWP 

prevalence were examined by mine size (i.e., 

employment). The hypothesis investigated was 

that smaller mines lack resources in many areas for the full protection of workers, including 

dust suppression and up-to-date knowledge of 

means to prevent disease development. (It may 

also be that smaller mines tend to be those mining the thinner coal seams.) The results show 

that CWP prevalence is increasing in mines of 

all sizes, but the trend is much more obvious 

and much greater among miners employed in 

smaller coal mines. 

Of the other factors listed above that may be 

contributing to the rise in CWP prevalence, 

increased working hours gives rise to special 

concern. Overall, U.S. coal miners are working longer hours. Figure 10, derived from data 

collected by MSHA shows a steady increase 

in the number of hours worked. This increase 

appears to arise from not only working longer 

shifts (e.g., 10 or 12 hours), but from working 

on weekends as well. Although no epidemiologic data exist that implicate longer hours as 
16 NIOSH CIB 64 • Coal Mine Dust Exposures

a contributory causative factor for CWP, working longer hours leads to the inhalation of more 

dust into the lungs. For example, working 12 

hours leads to 50% more dust entering the lung 

compared to a regular 8-hour shift, assuming 

all other factors are equal (e.g., exposure concentration and breathing rates). Additionally, 

working longer workshifts reduces the time 

available between workshifts for the process of 

clearing the dust deposited in the lungs. Unfortunately, the available information on working 

hours in U.S. coal miners is not miner-specific 

but rather by coal mine, substantially reducing 

the validity of a formal analysis of this hypothesis. A report on British miners concluded that 

longer working hours were a factor in causing 

an increase in CWP prevalence at two mines 

(36). In the CCD, NIOSH recommended reducing dust exposures below the 1 mg/m3

 REL 

for work shifts exceeding 40 hr/week (using 

the method of Brief and Scala (37)). This approach has also been recommended for British 

coal mines (38). 

Finally, productivity per hour worked also 

increased from 1978–2000, although it has 

since declined (Figure 11). Of course, these 

increases in productivity (and, presumably, increased potential for dust generation) should 

have been met by commensurate increases in 

dust prevention measures (e.g., ventilation and 

water sprays) in order to maintain compliance 

with the permissible exposure limit. Superficially, the current data appear to confirm this, 

in that airborne dust levels have apparently not 

risen during that period (Figure 12). However, 

the veracity of coal mine dust data has been 

challenged in the past (39). Moreover, the discovery of abnormal white centers in the dust 

sampling filters prompted a special inspection 

Figure 10. Hours worked per underground coal miner, 1978–2008. (Source: http://www.msha.gov/

ACCINJ/BOTHCL.HTM).
NIOSH CIB 64 • Coal Mine Dust Exposures 17

Figure 11. Tons produced per hour worked at underground coal mines. 1978–2008. (Source: http://

www.msha.gov/ACCINJ/BOTHCL.HTM).

Figure 12. Respirable coal mine dust: Geometric mean exposures by type of mine (UG=underground, 

SU=surface), MSHA inspector (INSP) and mine operator (OPER) samples. [MSHA coal mine inspector and mine operator dust data].
18 NIOSH CIB 64 • Coal Mine Dust Exposures

program (40) that showed that dust levels from 

operator samples consistently were lower than 

those from MSHA inspector samples, and that 

these differences were greater the smaller the 

mine (Figure 13). As with hours worked, there 

is a lack of reliable productivity data linkable 

with the health outcome data in order to investigate this issue further.

2.3 Mortality

A report on temporal patterns in pneumoconiosis mortality in the U.S. showed a substantial decline in numbers of deaths from CWP between 

1968 and 2000 (41). This decline is consistent 

with the reductions in dust level mandated by 

the 1969 Coal Mine Act. A major additional 

factor contributing to the declining number of 

CWP deaths is the diminishing coal mining 

workforce in the U.S. Figure 14 (Figure 1, from 

CDC (42)) shows the CWP death rate results 

extended to 2006. A similar situation has been 

observed in other developed countries, e.g., 

Australia (26). Recent U.S. results have shown, 

however, a disconcerting increase in years of 

potential life lost (YPLL) due to CWP in the 

U.S. since 2002 (42). Not only has the YPLL 

been increasing in younger CWP decedents 

(<65 years old), but the YPLL per CWP decedent has also been increasing over those same 

years (Figure 15; Figure 2 from CDC (42)). 

This may be related to the observed increase 

in CWP prevalence observed in recent years as 

noted earlier. 

The post-1995 period saw the publication of a 

number of mortality analyses that augmented 

the earlier mortality findings on coal miners. 

Figure 13. Ratio of special inspection sample values to preceding operator compliance sample values by mine size. (Source: MSHA Report of the Statistical Task Team of the Coal Mine Respirable 

Dust Task Group. (40)).
NIOSH CIB 64 • Coal Mine Dust Exposures 19

Figure 14. Age-adjusted death rates (per million) for decedents age ≥25 years with coal workers’ 

pneumoconiosis as the underlying cause of death—United States, 1968–2006. (Source: CDC (42)).

Figure 15. Years of potential life lost (YPLL) before age 65 and mean YPLL per decedent for decedents aged ≥25 years with coal workers’ pneumoconiosis as the underlying cause of death—United 

States, 1968–2006. (Source: CDC (42)).
20 NIOSH CIB 64 • Coal Mine Dust Exposures

Most of those studies outside of the United 

States and United Kingdom did not have 

quantitative measurements of dust exposure. 

However, they do support previous findings 

concerning the overall increased mortality of 

coal miners and the additional risk imposed 

by the development of CWP (43–45). Studies 

using quantitative exposures showed that mortality from CWP increased with increasing 

cumulative exposure to coal mine dust (46). 

The British study (47) included exposure estimates for respirable quartz; cumulative exposure to respirable coal mine dust and respirable 

quartz were each highly significant predictors 

of pneumoconiosis mortality, although the 

relationship was stronger with coal dust than 

quartz. Respirable quartz exposure was associated with a small but statistically significant 

relative risk for lung cancer mortality (47). 

2.4 Toxicology

Although coal mine dust and crystalline silica dust remain the two exposures of primary 

concern for environmental control, the post1995 period has seen the publication of results 

from analyses aimed at eliciting information 

on what constituents of coal mine dust predict 

CWP development. These include: 1) free radicals, in which particles from freshly-fractured 

siliceous rock have been found to be more fibrogenic than aged particles (48); 2) particle 

occlusion, in which clay present in the rock 

strata can surround the silica particles and 

render them less toxic (49); and 3) bioavailable iron, which has been found to predict coal 

mine dust toxicity (50, 51). 

McCunney et al. (52), favored the third explanation (bioavailable iron) and downplayed the 

role of quartz in the etiology of coal workers’ 

pneumoconiosis. However, in an analysis of lung 

inflammatory cell counts from bronchoalveolar 

lavage in coal miners and non-miners, Kuempel et al. (53) showed that quartz dust (as either cumulative exposure or estimated lung 

burden) was a significant predictor of pulmonary inflammation and radiographic category 

of simple CWP. Cumulative coal dust exposure 

did not significantly add to those predictions, 

which may have been due to the high correlation between the coal and quartz cumulative 

exposures, such that separate effects for these 

two dusts could not be clearly demonstrated. 

Against this, epidemiologic research has not 

demonstrated a strong effect of crystalline silica on CWP development in situations where 

silica levels are low. Rather, the level of coal 

mine dust, per se, has been the strongest predictor of CWP. However, the work of Laney et 

al. (34), as noted above, showed clear evidence 

of an increase in r-type radiographic opacities 

(typically associated with silicosis) and rapid 

progression of pneumoconiosis among U.S. 

coal miners in Kentucky, Virginia, and West 

Virginia, suggesting that they were exposed to 

excessive levels of respirable crystalline silica, 

and were thus at risk of silicosis. As noted previously, dust sampling results support this hypothesis (23). There is, therefore, the clear need 

to minimize exposure to silica dust, especially for those jobs involving drilling or cutting 

sandstone and other siliceous rock. Moreover, 

as noted above, this is particularly pertinent 

because changing mining conditions might be 

leading to an increase in the potential for exposure to silica dust. 

Page and Organiscak (54) linked the issue of 

coal rank, a known risk factor for CWP development in the U.S., Britain, and Germany, with 

the potential for higher levels of free radicals 

to be encountered where such coals are mined, 

and noted above by Dalal (48) and others to 

have greater levels of cytotoxicity. 
NIOSH CIB 64 • Coal Mine Dust Exposures 21

2.5 Risk Analysis

Kuempel et al. (13) describe in more detail the 

risk analyses provided in the NIOSH CCD, including the excess (exposure-attributable) prevalence of CWP and PMF in underground coal 

miners exposed to various levels of coal mine 

dust for a working lifetime (as shown in the 

CCD and also presented here in Table 1). More 

recent risk estimates have been provided from 

research on British coal miners (Figure 16, from 

Figure 1 of Soutar et al. (55)). The latter apply 

to coal composed of 86.2% carbon (coal rank) 

and to underground coal miners who work 40 

years at the designated coal mine dust level. 

Risks of PMF range from 0.8% at 1.5 mg/m3 to 

about 5% at 6 mg/m3, while risks of category 2 

or greater CWP range from about 1.5% at 1.5 

mg/m3 to about 9% at 6 mg/m3. Note that due to 

the different ways in which the risk estimates are 

derived, these are not directly comparable with 

those from U.S. studies shown in Table 1. However, the findings are consistent with those from 

U.S. studies in indicating that even at the lower 

coal mine dust levels recommended by NIOSH, 

and as noted in the CCD, some incidence of 

CWP would still be expected, especially among 

miners of higher rank coal. 

Soutar et al. (55) also provide information on 

the risk of silicosis in underground coal miners. 

Their findings were developed from observations at one mine in which unusually high concentrations of crystalline silica dust occurred 

periodically (56). In their analysis, the authors 

chose to divide the analysis between exposures 

< 2 mg/m3 and ≥ 2 mg/m3. This dichotomy, in 

the authors’ presentation, was associated with 

more rapid development of silicosis in the ≥ 2 

mg/m3 exposure range compared to chronic silicosis development at exposures < 2 mg/m3

. The 

findings indicate that short excursions to high 

silica dust intensities are considerably more 

hazardous than the same level of cumulative 

exposure at a lower intensity. They therefore 

demonstrate that mining situations involving 

the cutting of rock should be avoided if at all 

possible, or if necessary, that all precautions 

should be taken to minimize dust exposures. 

The findings for <2 mg/m3 (which apply to 

most coal mining environments that do not 

involve direct rock cutting) are given in Figure 

17 (Figure 3 of Soutar et al. (55)).

Figure 16. Risks at age 58–60 after 35–40 

working years of: PMF; category 2 or greater 

(2+); 993 ml deficit of FEV1 in nonsmokers; 

993 ml deficit of FEV1 in smokers. (Source: 

Soutar et al. (55)).

Figure 17. Risks for category 2 silicosis in relation to respirable silica concentration (<2 mg/

m3) averaged over 15 years. (Source: Soutar et 

al. (55)).

NIOSH CIB 64 • Coal Mine Dust Exposures 23

3 Other Respiratory Disease Outcomes

A recently published mortality study from the 

United States (46) comprised a longer followup of a study on the same cohort of underground coal miners published in 1995 (69). 

It showed that mortality from chronic airway 

obstruction (CAO) was elevated. Smoking, 

pneumoconiosis, coal rank region, and cumulative coal mine dust exposure were all predictors of mortality from CAO. Dust exposure effects were observed within the never-smoker 

subset of the cohort. The observed dust-related 

relative risks for CAO were similar to those for 

pneumoconiosis. The findings showed dustrelated effects for chronic bronchitis and emphysema as well as CAO. A recent British study 

re-affirmed that mortality from COPD was related to coal mine dust exposure (47). Finally, 

the implications of COPD (due to coal mine 

dust exposure as well as smoking) in causing 

increased mortality was explored by examining mortality risk in relation to rates of ventilatory function decline in coal miners (70). Rates 

of ventilatory decline 2–3 times the normal 

age-related decline were associated with distinct increases in subsequent mortality. 

Past pathologic studies have shown that emphysema severity in coal miners is related to 

dust exposure. Recent studies on South African 

and U.S. coal miners confirmed these findings 

(71, 72). Important additional information on 

this topic, using quantitative estimates of both 

coal mine dust exposure and smoking amount, 

has been recently published by Kuempel et al. 

(73). These authors found a highly significant 

relationship between cumulative exposure 

to respirable coal mine dust and emphysema 

severity at autopsy, controlling for effects of 

Coggon and Taylor (57), in an extensive review, concluded that the “...balance of evidence points overwhelmingly to an impairment of lung function from exposure to coal 

mine dust, and this is consistent with the increased mortality from COPD that has been 

observed in coal miners.” Findings on COPD 

and related outcomes in coal miners since 1995 

(58–64) have continued to support their conclusion (which was largely based on pre-1995 

information). The findings have also identified 

other risk factors in coal mining for pulmonary disease development. These include work 

in roof bolting, exposure to explosive blasting 

fumes, and exposure to dust control spray water previously stored in holding tanks (65). 

The post-1995 findings have also elucidated 

patterns of lung function decline in coal miners, indicating that new miners tend to suffer 

more severe declines on starting work, after 

which the declines attenuate somewhat. This 

finding, derived initially from the analysis by 

Seixas et al. (66), was explored further by Henneberger and Attfield (58), who confirmed that 

the temporal pattern of lung function decline 

was different in newly-hired coal miners as 

compared to experienced miners. A possible 

reason for this could be a healthy worker survival effect. A study to explore this issue further, undertaken on new Chinese coal miners, 

confirmed that starting work in coal mining 

led to large initial drops in lung function, after 

which lung function declined at a lesser rate 

(67). In a follow-up analysis, the researchers 

reported that the development of respiratory 

symptoms consistent with bronchitis contributed to the early declines in lung function (68). 
24 NIOSH CIB 64 • Coal Mine Dust Exposures

smoking, age, and other variables. The effect of 

dust exposure was similar in magnitude to that 

of smoking, and was seen in the never-smoking subgroup. In a further analysis, Kuempel et 

al. established that exposure to coal mine dust 

can produce clinically important levels of emphysema in coal miners (74). 

The above findings support the CCD’s recommendation to reduce the permissible coal mine 

dust exposure limit in underground coal mines 

to prevent the development of COPD, the associated severe declines in lung function, and 

the ensuing premature mortality. 

There have been several reports of interstitial 

disease associated with exposure to coal mine 

dust, perhaps representing a manifestation of 

CWP, although little systematic research on 

this topic has been undertaken (75, 76).

3.1 Risk Analysis

Kuempel et al. (13) describe in more detail the 

risk analyses summarized in the NIOSH CCD, 

including the excess (exposure-attributable) 

prevalence of lung function deficits in underground coal miners exposed to various levels 

of coal mine dust for a working lifetime (CCD 

Table 4–7 (1); Table 2). More recent risk estimates from research on U.K. coal miners have 

been published (Figure 15; Figure 1 of Soutar et 

al. (55)). They apply to coal composed of 86.2% 

carbon (coal rank) and to underground coal 

miners who work 35 years at specified coal mine 

dust levels ranging from 1 to 6 mg/m3. Risks of a 

deficit of approximately 1 liter in forced expiratory volume in 1 second (FEV1

) among never 

smokers range from 10% at zero dust exposure to about 19% at 6 mg/m3

. The concomitant risks for smokers range from about 22% to 

36%, respectively. Note that due to the different ways in which the risk estimates have been 

derived, these are not directly comparable with 

those shown from U.S. studies shown in Table 

2. However, they are consistent with findings 

from U.S. studies in that even at the 1 mg/m3

coal mine dust exposure limit recommended 

by the CCD, some occupational effect on ventilatory function is expected.
NIOSH CIB 64 • Coal Mine Dust Exposures 25

4 Cancer Outcomes

weak relationship of silica exposure with lung 

cancer mortality (47). A recent development in 

this regard is the finding that lung-deposited 

silica or coal dust inhibits the induction of cytochrome P4501A1 by polycyclic aromatic hydrocarbons (PAH) (78–80). It is hypothesized 

that the resulting lower cytochrome activity 

might to some extent counteract the carcinogenic effects of tobacco smoke by limiting metabolism of PAH in tobacco smoke into carcinogenic metabolites. This may explain the lack 

of clear findings on dust exposure and lung 

cancer in coal mining.

There have been occasional reports of elevated 

stomach cancer mortality among coal miners. 

The post-1995 results from various reports 

have not confirmed these findings. In particular, no relationship was detected in the two 

studies having quantitative exposure measurements (46, 47). 

Two cancer outcomes—lung cancer and stomach cancer—have been of particular interest 

with respect to work in coal mining. Lung 

cancer has been suspected to arise in coal miners because of their exposure to crystalline 

silica dust, which has been determined to be a 

Group I carcinogen by the International Agency for Research on Cancer, at least in some 

occupational settings (77). However, findings 

in coal miners have been conflicting and have 

not strongly supported a relationship between 

coal mine dust exposure and lung cancer. The 

post-1995 findings continue this picture. No 

overall excess or relationship with increasing 

dust exposure was seen in lung cancer mortality in a study of U.S. underground coal miners 

(46). However, this study, lacking silica dust 

exposure measurements, could not effectively 

evaluate the hypothesis of interest. In contrast, 

a recent British study that did include cumulative crystalline silica dust exposures found a 

NIOSH CIB 64 • Coal Mine Dust Exposures 27

5 Dust Exposure Levels, Control, and Compliance

dust. The biggest reduction in reported levels 

was for coal mine dust at surface mines as sampled by inspectors (recent levels are ~40% of 

those around 1980). The smallest decline was 

for silica levels in underground mines, where 

there has been essentially no change over the 

time period (recent levels are ~98% of those 

in the early 1980s). Overall, levels of both coal 

mine dust and crystalline silica dust were reported to be higher in underground mines 

than in surface mines.

5.2 Dust Exposure Assessment

The primary advance since 1995 in the dust assessment arena has been the development of a 

5.1 Dust Exposure Levels

Overall trends in reported coal mine dust and 

crystalline silica exposure levels for the United 

States are shown in Figures 12 and 18. These 

follow the format of the 2007 WoRLD Surveillance Report (23) Figures 2–6 and 3–5a, but are 

updated to 2008. The data in both figures imply 

that dust levels have declined over time, with 

those from recent years being about 75% of 

those around 1980, overall. This has occurred 

over a time period when underground production levels from both longwall and continuous 

miner operations significantly increased. However, the reductions vary depending on the type 

of mine, the source of the data, and the type of 

Figure 18. Respirable quartz dust: Geometric mean exposures by type of coal mine (operator and 

inspector data combined). [MSHA coal mine inspector and mine operator dust data].
28 NIOSH CIB 64 • Coal Mine Dust Exposures

continuously-measuring personal dust monitor 

(PDM) (81). The PDM enables within-shift assessment of dust exposures, permitting prompt 

action to intervene and reduce excessive levels. Conventional practices that rely on the 

gravimetric assessment of dust collected on air 

sample filters preclude speedy remediation because the delay in obtaining results from the 

dust laboratory could mean that miners continue to be over-exposed before any indication 

of a problem is available from the laboratory 

results. The personal dust monitor is now a 

commercially available product and, as its use 

is adopted by mines, more timely and targeted 

interventions to reduce dust exposures will be 

possible. In 2010, the Mine Safety and Health 

Administration published new rules that provide for the approval and use of the PDM, in 

addition to the Coal Mine Dust Personal Sampler Unit, for determining the concentration of 

respirable dust in coal mine atmospheres (82). 

5.3 Compliance Policy

 and Procedures

The federal policies and procedures for regulating underground coal mine dust levels have 

been the subject of criticism from their introduction in 1969. Since 1995 further critiques 

have been published (83, 84). The first publication provided a historical review, the basic argument being that the problems were intrinsic 

to a process in which an industry essentially 

regulates itself (i.e., through performing the 

airborne sampling upon which citations are 

based). The second publication revisited an 

issue that was addressed in the NIOSH CCD, 

in which it was recommended that MSHA not 

apply any upward adjustment of the REL for 

instrument uncertainty. Information indicating that reported dust levels from mine operator sampling were systematically lower than 

those obtained by mine inspectors during unannounced visits to mines to measure exposures has been published by MSHA (40).
NIOSH CIB 64 • Coal Mine Dust Exposures 29

6 Surface Coal Mining

reported evidence of CWP among workers in 

the dustier jobs and an association with intensity 

of exposure (85). Dust exposures were generally 

<1 mg/m3. In the United States, a relationship 

between tenure in surface coal mining jobs and 

prevalence of CWP (ILO category 1/0 or greater, 

and PMF) was reported (16).

Studies published prior to the NIOSH CCD 

showed that U.S. surface coal miners (particularly workers on drill crews) were at risk of developing CWP (or silicosis). There was also evidence 

that ventilatory function was reduced in relation 

to the number of years worked as drill operators 

or helpers. Since the CCD, a British study has 

NIOSH CIB 64 • Coal Mine Dust Exposures 31

7 Summary

pational respiratory disease among coal 

miners remains essentially unaffected 

by the newer findings that have emerged 

since publication of the CCD. 

New findings of particular note are:

1. After a long period of declining CWP 

prevalence, recent federal surveillance 

data indicate that the prevalence is rising. 

2. Coal miners are developing severe CWP 

at relatively young ages.

3. There is some indication that the mortality of younger coal miners from CWP 

is increasing. These workers would have 

been employed all of their working lives 

in environmental conditions mandated 

by the 1969 Coal Mine Act.

4. The pattern of CWP occurrence across 

the nation is not uniform; hot spots of 

disease appear to be concentrated in the 

central Appalachian region of southern 

WV, eastern KY, and western VA.

5. The cause of this resurgence in disease is 

likely multifactorial. Possible explanations 

include excessive exposure due to increases in coal mine dust levels and duration of 

exposure (longer working hours), and increases in crystalline silica exposure (see 

below). As indicated by data on disease 

prevalence and severity, workers in smaller mines may be at special risk.

6. Given that the more productive seams 

of coal are being mined out, a transition by the industry to mining thinner 

coal seams and those with more rock 

A considerable body of literature has been produced from studies of coal miners and the coal 

mining environment since 1995, both in the 

United States and elsewhere. Many of the newer publications, particularly those from other 

countries, lack quantitative dust exposure measurements, prohibiting full and valid examination of exposure-response relationships. Nevertheless, their findings all support early findings 

on British and U.S. coal miners, reinforcing the 

generally-accepted understanding that exposure to 

coal mine dust can give rise to various respiratory diseases, and that those diseases can cause 

disability and premature mortality. The remainder of the newer publications that do have quantitative exposure data report findings that refine 

or augment the fundamental exposure-response 

results summarized in the CCD. 

Overall, the following conclusions can be made:

1. No new findings have emerged since 1995 

that contradict the basic summarization 

of the respiratory health effects of coal 

mine dust and their relationship with dust 

exposures described in the CCD (1).

2. No new findings have emerged that substantially modify the basic understanding of coal mine dust exposure and its 

impact on respiratory health described 

in the CCD.

3. The new findings that have emerged 

strengthen prior results and also refine 

or add further knowledge on disease patterns and etiology described in the CCD.

4. Overall, the logical basis for recommendations concerning prevention of occu-
32 NIOSH CIB 64 • Coal Mine Dust Exposures

intrusions is taking place and will likely 

accelerate in the future. Concomitant 

with this is the likelihood of increased 

potential for exposure to crystalline silica, and associated increased risk of silicosis, in coal mining.

In summary, every effort needs to be made to 

reduce exposures both to respirable coal mine 

dust and to respirable crystalline silica. As recommended in the CCD, the latter task requires 

establishing a separate compliance standard in 

order to effectively limit exposure to silica dust. 
NIOSH CIB 64 • Coal Mine Dust Exposures 33

References

1. National Institute for Occupational Safety 

and Health. [1995]. Criteria for a recommended standard: Occupational exposure 

to coal mine dust. DHHS (NIOSH) Publication No. 95–106. Washington, DC, National Institute for Occupational Safety and 

Health. 

2. Attfield MD, Wagner G [1992]. Respiratory disease in coal miners. In: Rom WN 

ed. Environmental and occupational medicine. Boston, MA: Little, Brown and Company, pp. 325–344.

3. International Labour Office [1980]. International classification of radiographs of 

pneumoconiosis 1980 edition. Occupational Safety and Health Series no. 22 (Rev. 

80). Geneva: International Labour Office, 

pp. 1–48.

4. Jacobsen M, Rae S, Walton WH, Rogan 

JM [1971]. The relation between pneumoconiosis and dust exposure in British coal 

mines. In: Walton WH ed. Inhaled particles 

III. Old Woking, England: Unwin Brothers, 

pp. 903–919.

5. Hurley JF, Maclaren WM. [1987]. Dustrelated risks of radiological changes in 

coalminers over a 40-year working life: Report on work commissioned by NIOSH. 

TM/79/09. Edinburgh, Scotland, Institute 

of Occupational Medicine. 

6. Attfield MD, Seixas NS [1995]. Prevalence 

of pneumoconiosis and its relationship to 

dust exposure in a cohort of U.S. bituminous coal miners and ex-miners. Am J Ind 

Med 27:137–151.

7. Attfield MD, Morring K [1992]. An investigation into the relationship between coal 

workers’ pneumoconiosis and dust exposure in U.S. coal miners. Am Ind Hyg Assoc J 53:486–492.

8. Attfield MD, Hodous TK [1992]. Pulmonary function of U.S. coal miners related 

to dust exposure estimates. Am Rev Respir 

Dis 14:605–609.

9. Marine WM, Gurr D, Jacobsen M [1988]. 

Clinically important respiratory effects of 

dust exposure and smoking in British coal 

miners. Am Rev Respir Dis 137:106–112.

10. Soutar C, Campbell S, Gurr D, Lloyd M, 

Love R, Cowie H, Cowie A, Seaton A 

[1993]. Important deficits of lung function 

in three modern colliery populations—

relations with dust exposure. Am Rev 

Respir Dis 147:797–803.

11. Boehlecke B [1986]. Laboratory assessment 

of respiratory impairment for disability 

evaluation. DHHS (NIOSH) Publication 

No. 86–102. In: Merchant JA ed. Cincinnati, OH: U.S. Department of Health and 

Human Services.

12. ATS [1991]. Lung function testing: selection 

of reference values and interpretive strategies. Am Rev Respir Dis 144:1202–1218.

13. Kuempel ED, Smith RJ, Attfield MD, 

Stayner LT [1997]. Risks of occupational 

respiratory diseases among U.S. coal miners. Appl Occup Environ Hyg 12:823–831.

14. Seixas NS, Robins TG, Attfield MD, Moulton LH [1993]. Longitudinal and cross sectional analyses of exposure to coal mine 
34 NIOSH CIB 64 • Coal Mine Dust Exposures

dust and pulmonary function in new miners. Br J Ind Med 50:929–937.

15. U.S. Department of Labor [1996]. Report 

of the Secretary of Labor’s Advisory Committee on the Elimination of Pneumoconiosis among Coal Mine Workers. Washington, DC: US Department of Labor,

16. CDC [2003]. Pneumoconiosis prevalence 

among working coal miners examined in 

federal chest radiograph surveillance programs—United States, 1996–2002. MMWR 

Morb Mortal Wkly Rep 52:336–340.

17. CDC [2006]. Advanced cases of coal workers’ pneumoconiosis—two counties, Virginia, 2006. MMWR Morb Mortal Wkly 

Rep 55:909–913.

18. CDC [2007]. Advanced pneumoconiosis 

among working underground coal miners—

Eastern Kentucky and Southwestern Virginia, 2006. MMWR Morb Mortal Wkly 

Rep 56:652–655.

19. Laney AS, Attfield MD [2010]. Coal workers’ pneumoconiosis and progressive massive fibrosis are increasingly more prevalent among workers in small under ground 

coal mines in the United States. Occup Environ Med 67:428–431.

20. Loomis D [2010]. Basic protections are still 

lacking. Occup Environ Med 67:361.

21. Seaton A [2010]. Coal workers’ pneumoconiosis in small mines in the United States. 

Occup Environ Med 67:364.

22. Antao VC, Petsonk EL, Sokolow LZ, Wolfe 

AL, Pinheiro GA, Hale JM, Attfield MD 

[2005]. Rapidly progressive coal workers’ 

pneumoconiosis in the United States: geographic clustering and other factors. Occup Environ Med 62:670–674.

23. National Institute for Occupational Safety 

and Health [2008]. Work-related lung disease surveillance report 2007, Volume 1. 

DHHS (NIOSH) Publication No. 2008–143a. 

Cincinnati, OH, National Institute for Occupational Safety and Health. 

24. National Institute for Occupational Safety 

and Health [2010]. Work-related lung disease (WORLD) surveillance system. http://

www2a.cdc.gov/drds/WorldReportData/

25. Wade WA, Petsonk EL, Young B, Mogri I 

[2011]. Severe Occupational Pneumoconiosis Among West Virginia Coal Miners: 

138 Cases of Progressive Massive Fibrosis 

Compensated Between 2000–2009. Chest 

DOI 10.1378/chest. 10-1326:1–14.

26. Smith DR, Leggat PA [2006]. 24 years of 

pneumoconiosis mortality surveillance in 

Australia. J Occup Health 48:309–313.

27. Baur X, Latza U [2005]. Non-malignant 

occupational respiratory diseases in Germany in comparison with those of other 

countries. Int Arch Occup Environ Health 

78:593–602.

28. Naidoo RN, Robins TG, Solomon A, White 

N, Franzblau A [2004]. Radiographic outcomes among South African coal miners. 

Int Arch Occup Environ Health 77:471–481.

29. Marek K, Lebecki K [1999]. Occurrence 

and prevention of coal miners’ pneumoconiosis in Poland. Am J Ind Med 36:

610–617.

30. Nguyen AL, Matsuda S [1998]. Pneumoconiosis problem among the Vietnamese coal 

mine workers. J UOEH 20:353–360.

31. Parihar YS, Patnaik JP, Nema BK, Sahoo 

GB, Misra IB, Adhikary S [1997]. Coal 

workers’ pneumoconiosis: a study of prevalence in coal mines of eastern Madhya 
NIOSH CIB 64 • Coal Mine Dust Exposures 35

Pradesh and Orissa states of India. Ind 

Health 35:467–473.

32. Suarthana E, Laney AS, Storey E, Hale JM, 

Attfield MD. Coal Workers’ Pneumoconiosis in the United States: Regional Differences 40 Years after Implementation of the 

1969 Federal Coal Mine Health and Safety 

Act. Occup.Environ. Med 2011 (In Press)

33. Peters RH, Fotta B, Mallett LG [2001]. The 

influence of seam height on lost-time injury and fatality rates at small underground 

bituminous coal mines. Appl Occup Environ Hyg 16:1028–1034.

34. Laney AS, Petsonk EL, Attfield MD [2009]. 

Pneumoconiosis among under ground bituminous coal miners in the United States: 

is silicosis becoming more frequent? Occup Environ Med 

35. Pollock DE, Potts JO, Joy GJ [2010]. Investigation into dust exposures and mining 

practices in mines in the southern Appalachian Region. Mining Engineering 62: 

44–49.

36. Scarisbrick DA, Quinlan TR [2002]. Health 

surveillance for coal workers’ pneumoconiosis in the United Kingdom 1998–2000. 

Ann Occup Hyg 46 (Suppl. 1):254–256.

37. Brief RS, Scala RA [1975]. Occupa-tional 

exposure limits for novel work schedules. 

Am Ind Hyg Assoc J 36:467–469.

38. Kenny LC, Hurley F, Warren ND [2002]. 

Estimating the risk of contracting pneumoconiosis in the UK coal mining industry. Ann Occup Hyg 46(Suppl. 1):257–260.

39. Boden LI, Gold M [1984]. The accuracy of 

self-reported regulatory data: The case of 

coal mine dust. Am J Ind Med 6:–440.

40. U.S. Mine Safety and Health Administration [1993]. Report of the Statistical Task 

Team of the Coal Mine Respirable Dust 

Task Group. Washington DC: US Department of Labor,

41. CDC [2004]. Changing patterns of pneumoconiosis mortality—United States, 1968– 

2000. MMWR Morb Mortal Wkly Rep 

53:627–632.

42. CDC [2009]. Coal workers’ pneumoconiosis-related years of potential life lost before 

age 65 years—United States, 1968–2006. 

MMWR Morb Mortal Wkly Rep 58:1412–

1416.

43. Starzynski Z, Marek K, Kujawska A, Szymczak W [1996]. Mortality among coal miners with pneumoconiosis in Poland. Int J 

Occup Med Environ Health 9:279–289.

44. Yi Q, Zhang Z [1996]. The survival analyses of 2738 patients with simple pneumoconiosis. Occup Environ Med 53:129–135.

45. Meijers JM, Swaen GM, Slangen JJ [1997]. 

Mortality of Dutch coal miners in relation 

to pneumoconiosis, chronic obstructive 

pulmonary disease, and lung function. Occup Environ Med 54:708–713.

46. Attfield MD, Kuempel ED [2008]. Mortality among U.S. underground coal miners: A 23-year follow-up. Am J Ind Med 

51:231–245.

47. Miller BG, MacCalman L [2010]. Causespecific mortality in British coal workers 

and exposure to respirable dust and quartz. 

Occup Environ Med 67:270–276.

48. Dalal NS, Newman J, Pack D, Leonard S, 

Vallyathan V [1995]. Hydroxyl radical generation by coal mine dust: Possible implication to coal workers’ pneumoconiosis. 

Free Radic Biol Med 18:11–20.

49. Wallace WE, Keane MJ, Harrison JC, Stephens JW, Brower PS, Grayson RL, Attfield 
36 NIOSH CIB 64 • Coal Mine Dust Exposures

MD [1995]. Surface properties of silica 

in mixed dusts. In: Castranova V, Vallyathan V, Wallace WE eds. Silica and silicainduced lung diseases. Boca Raton: CRC 

Press, pp. 107–117.

50. Huang X, Li W, Attfield MD, Nadas A, 

Frenkel K, Finkelman RB [2005]. Mapping 

and prediction of coal workers’ pneumoconiosis with bioavailable iron content in the 

bituminous coals. Environ Health Perspect 

113:964–968.

51. Zhang Q, Dai J, Ali A, Chen L, Huang X 

[2002]. Roles of bioavailable iron and calcium in coal dust-induced oxidative stress: 

possible implications in coal workers’ lung 

disease. Free Radic Res 36:285–294.

52. McCunney RJ, Morfeld P, Payne S [2009]. 

What component of coal causes coal workers’ pneumoconiosis? J Occup Environ 

Med 51:462–471.

53. Kuempel ED, Attfield MD, Vallyathan V, 

Lapp NL, Hale JM, Smith RJ, Castranova V 

[2003]. Pulmonary inflammation and crystalline silica in respirable coal mine dust: 

dose-response. J Biosci 28:61–69.

54. Page SJ, Organiscak JA [2000]. Suggestion 

of a cause-and-effect relationship among 

coal rank, airborne dust, and incidence of 

workers’ pneumoconiosis. AIHAJ 61:785–

787.

55. Soutar CA, Hurley JF, Miller BG, Cowie 

HA, Buchanan D [2004]. Dust concentrations and respiratory risks in coalminers: 

key risk estimates from the British Pneumoconiosis Field Research. Occup Environ 

Med 61:477–481.

56. Buchanan D, Miller BG, Soutar CA [2005]. 

Quantitative relations between exposure to 

respirable quartz and risk of silicosis. Occup Environ Med 60:159–164.

57. Coggon D, Taylor AN [1998]. Coal mining and chronic obstructive pulmonary 

disease: a review of the evidence. Thorax 

53:398–407.

58. Henneberger PK, Attfield MD [1996]. Coal 

mine dust exposure and spirometry in experienced miners. Am J Respir Crit Care 

Med 153:1560–1566.

59. Henneberger PK, Attfield MD [1997]. Respiratory symptoms and spirometry in experienced coal miners: Effects of both distant and recent coal mine dust exposures. 

Am J Ind Med 32:268–274.

60. Carta P, Aru G, Barbieri MT, Avata-neo G, 

Casula D [1996]. Dust exposure, respiratory symptoms, and longitudinal decline in 

lung function in young coal miners. Occup 

Environ Med 53:312–319.

61. Beeckman LF, Wang ML, Petsonk EL, Wagner GR [2001]. Rapid declines in FEV1 

and subsequent respiratory symptoms, illnesses, and mortality in coal miners in the 

United States. Am J Respir Crit Care Med 

163:633–639.

62. Naidoo RN, Robins TG, Becklake M, Seixas 

N, Thompson ML [2007]. Cross-shift peak 

expiratory flow changes are unassociated 

with respirable coal dust exposure among 

South African coal miners. Am J Ind Med 

50:992–998.

63. Naidoo RN, Robins TG, Seixas N, Lalloo 

UG, Becklake M [2006]. Respirable coal 

dust exposure and respiratory symptoms 

in South-African coal miners: a comparison of current and ex-miners. J Occup Environ Med 48:581–590.

64. Naidoo RN, Robins TG, Seixas N, Lalloo UG, 

Becklake M [2005]. Differential respirable 

dust related lung function effects between 

current and former South African coal 
NIOSH CIB 64 • Coal Mine Dust Exposures 37

miners. Int Arch Occup Environ Health 

78:293–302.

65. Wang ML, Petsonk EL, Beeckman LF, Wagner GR [1999]. Clinically important FEV1 

declines among coal miners: an exploration of previously unrecognized determinants. Occup Environ Med 56:837–844.

66. Seixas NS, Robins TG, Attfield MD, 

Moulton LH [1992]. Exposure-response 

relationships for coal mine dust and obstructive lung disease following enactment 

of the Federal Coal Mine Health and Safety 

Act of 1969. Am J Ind Med 21:715–734.

67. Wang ML, Wu ZE, Du QG, Petsonk EL, 

Peng KL, Li YD, Li SK, Han GH, Attfield 

MD [2005]. A prospective cohort study 

among new Chinese coal miners—The early pattern of lung function change. Occup 

Environ Med 62:800–805.

68. Wang ML, Wu Z-E, Du Q-G, Peng K-L, Li 

Y-D, Li S-K, Han G-H, Petsonk EL [2007]. 

Rapid decline in forced expiratory volume 

in 1 second (FEV1) and the development 

of bronchitic symptoms among new Chinese coal miners. J Occup Environ Med 

49:1143–1148.

69. Kuempel ED, Stayner LT, Attfield MD, 

Buncher CR [1995]. Exposure-response 

analysis of mortality among coal miners in 

the United States. Am J Ind Med 28:167–184.

70. Sircar K, Hnizdo E, Petsonk E, Attfield M 

[2007]. Decline in lung function and mortality: implications for medical monitoring. Occup Environ Med 64:461–466.

71. Naidoo RN, Robins TG, Murray J [2005]. 

Respiratory outcomes among South African coal miners at autopsy. Am J Ind Med 

48:217–224.

72. Vallyathan V, Green FHY, Brower P, Attfield M [1997]. The role of coal mine dust 

exposure in the development of pulmonary 

emphysema. Ann Occup Hyg 41:352–357.

73. Kuempel ED, Wheeler MW, Smith RJ, Vallyathan V, Green FH [2009]. Contributions 

of dust exposure and cigarette smoking to 

emphysema severity in coal miners in the 

United States. Am J Respir Crit Care Med 

180:257–264.

74. Kuempel ED, Vallyathan V, Green FHY 

[2009]. Emphysema and pulmonary impairment in coal miners: Quantitative relationship with dust exposure and cigarette 

smoking. Journal of Physics Conference 

Series 151:1–8.

75. Brichet A, Wallaert B, Gosselin B, RemyJardin M, Voisin C, Lafitte JJ, Tonnel AB 

[1997]. Primary diffuse interstitial fibrosis in coal miners: a new entity? Rev Mal 

Respir 14:277–285.

76. Brichet A, Tonnel AB, Brambilla E, Devouassoux G, Remy-Jardin M, Copin MC, 

Wallaert B [2002]. Chronic interstitial 

pneumonia with honeycombing in coal 

workers. Sarcoidosis Vasc Diffuse Lung Dis 

19:211–219.

77. International Agency for Research on Cancer. [1997]. IARC monographs on the evaluation of carcinogenic risks to humans: 

silica, some silicates, coal dust, and paraaramid fibrils, pp. 337–406. Geneva, Switzerland, World Health Organization, International Agency for Research on Cancer. 

78. Battelli LA, Ghanem MM, Kashon ML, 

Barger M, Ma JY, Simokevitz RL, Miles 

PR, Hubbs AF [2008]. Crystalline silica 

is a negative modifier of pulmonary cytochrome P-4501A1 induction. J Toxicol Environ Health 71:521–532.
38 NIOSH CIB 64 • Coal Mine Dust Exposures

79. Ghanem MM, Batteli LA, Mercer RR, 

Scabilloni JF, Kashon ML, Ma JY, Nath J, 

Hubbs AF [2006]. Apoptosis and Bax expression are increased by coal dust in the 

polycyclic aromatic hydrocarbon-exposed 

lung. Env Health Perspect 114:1367–1373.

80. Ghanem MM, Porter D, Batteli LA, Vallyathan V, Kashon ML, Ma JY, Barger MW, 

Nath J, Castranova V, Hubbs AF [2004]. 

Respirable coal dust particles modify cytochrome P4501A1 (CYP1A1) expression in 

rat alveolar cells. Am J Respir Cell Mol Biol 

31:171–183.

81. Page SJ, Volkwein JC, Vinson RP, Joy GJ, 

Mischler SE, Tuchman DP, McWilliams 

LJ [2008]. Equivalency of a personal dust 

monitor to the current United States coal 

mine respirable dust sampler. J Environ 

Monit 10:96–101.

82. U.S. Department of Labor [2010]. 30 

CFR Part 74 RIN 1219-AB61 Coal Mine 

Dust Sampling Devices. Federal Register 

75:17512–17529.

83. Weeks JL [2003]. The fox guarding the 

chicken coop: Monitoring exposure to respirable coal mine dust, 1969–2000. Am J 

Public Health 93:1236–1244.

84. Weeks JL [2006]. The Mine Safety and 

Health Administration’s criterion threshold 

value policy increases miners’ risk of pneumoconiosis. Am J Ind Med 49:492–498.

85. Love RG, Miller BG, Groat SK, Hagen S, 

Cowie HA, Johnston PP, Hutchison PA, 

Soutar CA [1997]. Respiratory health effects of opencast coalmining: a cross sectional study of current workers. Occup Environ Med 54:416–423.

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