Coal Dust Exposure and Mortality From
 

Ischemic Heart Disease Among a Cohort of
 

U.S. Coal Miners
 

Deborah D. Landen, MD, PhD,

1* Linda McWilliams, MS,1

1

Office of Mine Safety and Health Research, National Institute for Occupational Safety

and Health,Pittsburgh,Pennsylvania

James T. Wassell, PhD,

2

2

Division of Safety Research, National Institute for Occupational Safety and Health,

Morgantown,West Virginia

and Ami Patel, PhD, MPH3

3

Office of Public Health Preparedness and Response, Centers for Disease Control and

Prevention,Philadelphia,Pennsylvania

*Correspondence to: Deborah D. Landen, MD, PhD, Office of Mine Safety and Health

Research, National Institute for Occupational Safety and Health, 626 Cochrans Mill Road,

Pittsburgh,PA15236. E-mail: dlanden@cdc.gov

Background Particulate exposure from air pollution increases the risk of ischemic

heart disease (IHD) mortality. Although coal miners are highly exposed to coal dust

particulate, studies of IHD mortality risk among coal miners have had inconsistent

results. Previous studies may have been biased by the healthy worker effect.

Methods We examined the dose–response relationship between cumulative coal dust

exposure, coal rank, and IHD mortality among a cohort of underground coal miners

who participated in the National Study of Coal Workers’ Pneumoconiosis.

Results After adjusting for age, smoking, and body mass index, risk of IHD mortality

increased at higher levels of coal dust exposure. Mortality risk was also associated

with coal rank region.

Conclusion There was an increased risk of mortality from IHD associated with cumulative exposure to coal dust, and with coal rank. The effect of coal rank may be due

differences in the composition of coal mine dust particulate. The association of risk of

IHD mortality with cumulative particulate exposure is consistent with air pollution

studies. Am. J. Ind. Med. © 2011 Wiley-Liss, Inc.

KEY WORDS: coal dust; ischemic heart disease; mortality

INTRODUCTION	 

Particulate matter in air pollution is known to increase

the risk of cardiovascular morbidity and mortality [Dockery et al., 1993; Schwartz, 1999, 2001; Laden et al., 2000;

Pope et al., 2004; Vermylen et al., 2005; Ostro et al.,

2006]. Although coal miners are exposed to high concentrations of particulate from coal mine dust, studies which

have examined the risk of ischemic heart disease (IHD)

mortality among coal miners have had inconsistent results.

Some have shown a risk no different, or lower than that

of the general population [Rockette, 1977; Christie et al.,

1995; Une et al., 1995], while others have shown increased risk, either overall, or among subgroups [Liddell,

1973; Costello et al., 1975; Atuhaire et al., 1986; Meijers

et al., 1997; Attfield and Kuempel, 2008; Miller and

MacCalman, 2010].

Most previously published studies of IHD among coal

miners have used Standardized Mortality Ratios to compare their risk to that of general populations. These studies

may have been biased by the healthy worker effect, since

employed populations often experience lower mortality

than the general population [Fox and Collier, 1976]. Bias

from the healthy worker effect can be reduced by the use

of study designs which use internal comparison groups

[Gilbert, 1982]. A recent study of a large cohort of British

coal miners [Miller and MacCalman, 2010] used Cox’s

proportional hazards model to examine the risk of coal
2

dust and quartz exposure on IHD mortality within the cohort. Coal dust exposure (lagged 15 years) was associated

with IHD mortality when quartz exposure was included in

the model.

We examined IHD mortality risk among a cohort of

coal miners who had participated in the National Study of

Coal Workers’ Pneumoconiosis [Attfield and Morring,

1992] during 1969–1971, by comparing risk among miners with varying levels of dust exposure. We also examined the effect of coal rank, a factor associated with risk

of pneumoconiosis. Coal rank is a measure of coalification, the bio- and geochemical process which transforms

plant materials into coal [Coal Utilization, 2011]. Higher

and lower ranked coals differ in their physical and chemical properties. Since the physical and chemical composition of particulates influence their risks for the

development of chronic health conditions, including IHD

[Franklin et al., 2008; Ostro et al., 2008] we considered

coal rank to be a potential risk factor for IHD among this

cohort.

METHODS

Study Population

The cohort included 9,078 working underground coal

miners who had participated in medical examinations during the first round of the National Study of Coal Workers’

Pneumoconiosis (NSCWP) from 1969 through 1971. The

first round of the NSCWP was designed to estimate

the prevalence of pneumoconiosis among coal miners in

the United States [Morgan et al., 1973]. Thirty-one underground coal mines in ten states were chosen to represent

all major U.S. coal fields and mining methods. Miner participation was reported as 90.5%; all participating miners

signed consent forms for their participation in the study.

Data on demographics, smoking, and work history were

collected by questionnaire. Participants were given medical examinations, which included collection of data on

height and weight, as well as chest radiographs and pulmonary function tests. Of the 9,078 miners, 107 were excluded because of missing or invalid data on one or more

of vital status, smoking, or coal dust exposure.

Vital Status and Cause of Death

Follow-up of vital status through 1993 was determined through the Social Security Administration, the files

of the United Mine Workers of America Welfare and Retirement Fund, state Vital Statistics offices and the National Death Index database. The underlying cause of death on

the death certificate was classified according to the International Classification of Diseases, Revision 8 (ICD-8) for

deaths through 1979, and Revision 9 (ICD-9) for deaths

from 1980 to 1993. Deaths categorized as IHD were codes

410–414 in both ICD-8 and ICD-9. For pneumoconiosis

deaths, codes were 515, 515.0, 515.1, and 515.9 in ICD-8,

and 500, 502, and 505 in ICD-9.

Measurement of Exposure

Estimates of cumulative individual exposure to respirable coal mine dust were derived from each miner’s work

history up until the time of study enrollment. Using a jobexposure matrix, the time worked in each job title was

multiplied by a job title-specific exposure estimate, and

the result summed across all jobs. The job title-specific

exposure estimates came from two sources: surveys undertaken by the U.S. Bureau of Mines between 1968 and

1969, which obtained dust samples from 17 of the mines

which later participated in the NSCWP; and dust samples

collected in the mines between 1969 and 1971 by coal

mine operators and processed by the Mine Safety and

Health Administration (MSHA) under their compliance

program [Schlick, 1971]. The methodology for estimation

of dust exposure is described by Attfield and Morring

[1992] and by Seixas et al. [1990].

Coal rank region was assigned based on the location

of the mine in which the miner worked at the start of

follow-up. We grouped mines into the coal rank regions

described in previous studies of this cohort [Attfield

and Morring, 1992; Kuempel et al., 1995; Attfield and

Kuempel, 2008]. Two mines in eastern Pennsylvania

mined anthracite coal. Mines in other areas all mined

bituminous coals, but the coals differed by region in their

volatile content and percentage carbon, with higher ranked

coals in the east and lower ranked in the west. The bituminous coals are identified simply by their geographic

region: Eastern Appalachian, Western Appalachian,

Midwest, and West.

Statistical Analysis

Death from IHD and death from pneumoconiosis are

both known to be associated with particulate exposure.

Deaths from these two causes represent non-independent

competing risks. A competing risks situation arises when

an individual can experience more than one type of event

which could result in his removal from a cohort [David

and Moeschberger, 1978]. In this case, although our cause

of death of interest was IHD, miners may have been removed from the cohort by death from pneumoconiosis, for

which coal miners have a substantial increased mortality

risk [Morgan et al. 1973; Kuempel et al. 1995; Attfield

and Kuempel 2008], or from other non-IHD causes.

In order to accommodate the effect of competing

causes of mortality, we used a regression method for competing risks developed by Fine and Gray, which models
3

the effect of covariates on the cumulative incidence function (CIF) by a proportional hazards regression model

[Fine and Gray, 1999]. Unlike Cox proportional hazards

regression, which assumes non-informative censoring of

causes of death other than the cause of interest, the Fine–

Gray regression model accounts for the distribution of a

competing risk from other causes of death. Models using

the CIF provide a better estimator in a competing risks

situation [Pepe and Mori, 1993; Lau et al., 2009; Grambauer et al., 2010].

Analyses were conducted using the cmprisk package

[Gray, 2010] in R software [R Development Core Team,

2011]. Time at risk was calculated from the date of the

baseline examination to either date of death or study end.

To examine the relationship between dust exposure and

IHD mortality, as well as the effect of competing mortality

risks, we first generated CIF plots for deaths from IHD by

exposure level within each coal region. We tested for differences between exposure groups, comparing the results

obtained from the log rank test, which does not include

the effects of competing risks, with those obtained from

the Gray test, which does include the effects of competing

risks. Comparison of the results of these two tests has

been recommended by Pintilie [2006] as a way of assessing the importance of a competing risk.

We then fitted competing risks regression models to

estimate the effect of coal dust exposure and coal rank

region on IHD mortality, adjusted for body mass index,

pack-years of smoking, and age. For this analysis, the

Midwest and West coal regions, which had similar low

risk, were combined. Cumulative exposure was modeled

as each of the following: (1) a continuous linear variable,

(2) a continuous linear variable with the addition of a quadratic term, and (3) a categorical variable defined as quartiles of cumulative exposure. Competing risks were all

other causes of mortality, including pneumoconiosis. We

compared model fit using likelihood ratio tests.

We tested for interactions between confounders (age,

smoking, and body mass index) and exposure, and between coal region and exposure, using the likelihood ratio

test. We tested the validity of the proportional hazards

model assumption (that the hazard ratio (HR) does not

change over time) using a time-dependent variable representing the interaction between time since start of followup and cumulative exposure.

We then fit a separate model using Cox regression,

after excluding the Anthracite region, and compared the

results to the Fine–Gray competing risks regression

model.

RESULTS

Table I shows characteristics of the cohort at study

entry during 1969–1971. Forty-six percent were current or

ex-smokers, and 56.5% had a body mass index (BMI) in

the overweight or obese range (>25). Age, BMI, smoking

prevalence, and cumulative dust exposure were highest

among miners in the Anthracite coal region. During the

follow-up period through 1993, 36% of the cohort (3,224)

died; 957 deaths (29.5%) were due to IHD; and 245

(7.6%) due to pneumoconiosis.

Figure 1 shows CIF plots for mortality from IHD in

the Anthracite region, and in the four bituminous regions.

The bituminous regions were combined for presentation,

since the CIFs for all four regions were quite similar.

In the bituminous regions, IHD mortality risk increased

with quartile of dust exposure. In the Anthracite region,

however, risk was highest in the second quartile of exposure, while risk in the highest quartile of exposure

was similar to that for the lowest quartile. This pattern

is probably due to the effect of a competing risk from

pneumoconiosis mortality, which was much higher in

the Anthracite region than in the bituminous regions

(Fig. 2). Although the log rank test showed a significant

difference in IHD mortality between exposure groups in

the Anthracite region (P 1⁄4 0.04) Gray’s test, which

includes the effect of the competing risk, showed no difference (P 1⁄4 0.10). The disparate results of these two

tests indicated that a competing risk was affecting the data

[Pintilie, 2006].

TABLE I. Characteristics of the National Study of Pneumoconiosis Cohortat Enrollment,1969^1970

Characteristic All coalrank regions Anthracite EasternAppalachian WesternAppalachian Midwest West

No.ofminers 8,971 519 1,354 4,923 1,219 956

Mean (SD) age,years 44.5(11.9) 51.6 (8.8) 43.4(11.4) 44.1(11.8) 44.1 (12.5) 44.7(12.9)

Race, %White 95.1 99.4 92.9 93.6 98.0 99.6

Bodymass index, %>25 kg/m3 56.5 62.6 51.3 57.2 61.5 50.8

Smoking status, %ever smoked 46.0 51.3 46.8 45.3 41.3 51.3

Mean (SD) pack-years ofsmoking 17.5(17.4) 23.4(20.3) 15.7(16.0) 17.6 (17.4) 19.0 (18.0) 14.5(16.1)

Mean cumulativecoal dustexposure,mg-yr/m3 64.4(46.4) 91.3(40.3) 62.7(42.8) 65.1(46.6) 57.0 (46.5) 58.6(47.7)

SD,standard deviation.
4

FIGURE 1. Cumulative incidence function for mortality from (ischemic heart disease) by quartile of dust exposure in the anthracite

and bituminous regions.

We next modeled the relationship between cumulative

dust exposure and IHD mortality using the Fine–Gray

competing risks method. The best fit was provided by a

model with exposure categorized in quartiles (likelihood

ratio test with 4 df P 1⁄4 0.03 compared to the model with

continuous linear exposure and a quadratic term). This final model is shown in Table II. There was a significant

interaction between coal dust exposure and coal region

(P 1⁄4 0.007). The HRs are presented by quartile of exposure within region, compared to a reference group consisting of the lowest quartile of dust exposure in the Western

Appalachian region. Estimates have been adjusted for age,

smoking, and BMI. In the Midwest–West region, point

estimates for the two highest quartiles were above the reference level, but only quartile 3 was significantly different

(HR 1.92, 95% CI 1.12, 3.28). In the Eastern and Western

Appalachian regions, risk was significantly above reference for quartiles 2–4, and increased with increasing levels of coal dust exposure in Western Appalachia. In the

Anthracite region, none of the HRs were statistically significant. There was no interaction between time since

study enrollment and cumulative exposure, indicating that

the proportional hazards assumption was met.

As expected, risk increased with increasing years of

age, BMI, and pack-years of smoking. The HR for age

was 1.07 (95% CI 1.06, 1.08) and the HR for BMI was

1.04 (95% CI 1.02, 1.06). The HR for smoking increased

for each level of exposure, with the highest HR, 1.56

(95% CI 1.28, 1.90), in the group with over 30 pack years

of smoking.

FIGURE 2. Cumulative incidence function for mortality from (pneumoconiosis) by quartile of dust exposure in the anthracite and

bituminous regions.
5

TABLE II. Fine^Gray Subdistribution Hazard Ratios(HRs)and 95% ConfidenceIntervalsforIschemic Heart DiseaseMortality by Quartiles of Coal

Dust Exposure* and Coal Rank, AdjustedforAge, BMI,and Smoking

Coalregionand Person-years No. HRand

dust quartile follow-up of cases 95%CI

WesternAppalachia

Q1 (reference group)a 40,061 20 1.00

Q2 37,262 98 1.75(1.06,2.89)

Q3 37,039 184 2.08(1.26,3.43)

Q4 35,282 252 2.26(1.37,3.75)

EasternAppalachia

Q1 10,442 7 1.35(0.58,3.15)

Q2 11,347 41 2.63(1.52,4.53)

Q3 11,578 32 2.38 (1.40,4.07)

Q4 7,905 98 2.29 (1.31,4.00)

Midwest/West

Q1 21,702 11 0.92(0.45,1.89)

Q2 18,637 53 1.46 (0.86,2.50)

Q3 13,415 66 1.92(1.12,3.28)

Q4 13,543 71 1.51 (0.87,2.61)

Anthracite

Q1 886 1 1.94 (0.27,13.81)

Q2 2,815 11 2.04 (0.96,4.33)

Q3 4,860 15 1.18(0.59,2.34)

Q4 6,043 11 0.43(0.20,0.92)

*

Cumulative coal dust exposure (mg-yr/m3) at study entry: 1st quartile: :20, 2nd
 

quartile: 20.1^63.5, 3rd quartile: 63.6^97.4,and 4th quartile:>97.4.
 a

Q1^Q4 1⁄4 quartiles1^4.
 

Table III shows the results of the Cox proportional

hazards regression, with the Anthracite region (the region

affected by competing mortality risk) excluded. In this

analysis, there was no interaction between coal region and

dust exposure. There was a significant increase in the HRs

for IHD mortality risk associated with higher quartiles of

dust exposure. HRs for the coal rank regions were not statistically significant, although point estimates were in the

same direction as in the competing risks regression; increased in the Eastern Appalachian region, and decreased

in the Midwest/West.

TABLE III. Cox Proportional Hazards Regression Hazard Ratios(HRs)

and 95% ConfidenceIntervalsforIschemic Heart DiseaseMortality by

Quartiles of Dust Exposure* and Coal Rank Region, Adjusted forAge, BMI,

and Smoking

Person-years No. of HR,

follow-up cases 95%CI

Dustexposure quartile

Q1(reference)

a 72,205 38 1.00

Q2 67,246 192 1.58(1.09,2.30)

Q3 62,032 282 1.81(1.23,2.66)

Q4 56,730 421 1.92(1.29,2.86)

Coalrank

WesternAppalachia(reference) 149,644 554 1.00

EasternAppalachia 41,272 178 1.18(0.99,1.41)

Midwest/West 67,297 201 0.75(0.64,0.88)

Anthraciteregion excluded.
 *

Cumulative coal dust exposure (mg-yr/m3) at study entry: 1st quartile: :20,
 

2nd quartile: 20.1^63.5, 3rd quartile: 63.6^97.4,and 4th quartile:>97.4.
 a

Q1^Q4 1⁄4 quartiles1^4.
 

DISCUSSION

In this analysis of data collected for the National

Study of Coal Workers’ Pneumoconiosis, we have shown

that the risk of IHD increased with cumulative exposure to

respirable coal mine dust. The strongest effect was seen in

the two Appalachian regions. Results were uninformative

in the Anthracite region, which had the smallest sample

size. In the other regions, the exposure–response effect for

coal dust did not increase linearly, but flattened out at

higher levels of exposure. This pattern has also been found

in studies of particulate air pollution, which show steep

dose–response effects on cardiovascular mortality at low

levels, with attenuation at higher levels [Pope et al.,

2009]. In addition, attenuation of effect at high dose in

occupational studies may occur due to biases, including

healthy worker survivor effects, and depletion of the susceptible population in long-term studies [Stayner et al.,

2003].

Particulate exposures to coal miners are far greater

than particulate exposures to the general population from

ambient air. The current Environmental Protection Agency

(EPA) 24-hr standard for particulate matter with a mass

median aerodynamic diameter of :2.5 mm (PM2.5) is

35 mg/m3

, and the 24-hr standard for particulate matter

with a mass median aerodynamic diameter of :10 mm

(PM10) is 150 mg/m3 [EPA, 2006]. The current standard

for respirable coal mine dust, which has a particle size

distribution in between that of PM2.5 and PM10, is

2,000 mg/m3 per work shift [U.S. Congress, 1969].

In view of the high exposure levels, the risk for IHD

mortality among coal miners is smaller than would be

expected on the basis of studies of atmospheric particulate

[Pope and Dockery, 2006], even given that respirable coal

mine dust exposures are more limited, since they occur

only at work. While both the healthy worker effect and

attenuation of risk at higher exposures may play a role in

the lower effect size for coal dust exposure, the most important factor is probably a difference in the particulate,

both in terms of particle size distribution and particle

composition. The particulate fraction under 2.5 mm

(PM2.5, fine particles) is most closely linked with IHD in
6

atmospheric pollution studies [Schwartz et al., 1996; Kan

et al., 2007; Puett et al., 2008]. Most particles of this size

in ambient air come from combustion sources. A small

portion of fine particulate in ambient air comes from crustal material; this portion, however, has not been associated

with an increased risk of either IHD [Laden et al., 2000]

or of all-cause mortality [Ozkaynak and Thurston, 1987]

in air pollution studies. Coal particulate is mechanically

generated, so the particle size distribution within PM10

would tend toward larger particles. Since coal comes from

earth’s crust, fine particulate coal dust might be expected

to be less hazardous than particulate of similar size derived from combustion, perhaps on the basis of a differing

particle composition.

The influence of particle composition on IHD mortality has been studied less than the influence of particle size.

We found the IHD mortality risk varied with coal rank, an

indicator of differences in the composition of coal dust. In

studies of pneumoconiosis among coal miners, higher coal

rank is associated with a significantly increased risk of

development of pneumoconiosis [Morgan et al., 1973;

Attfield and Morring, 1992; Attfield and Seixas, 1995] and

of pneumoconiosis mortality [Kuempel et al., 1995]. Differences in risk related to coal rank have not been studied

extensively, but may involve differences in particle charge,

which affects the degree to which dust penetrates the lung

[Page and Organiscak, 2000], as well as the iron content

of the coal [Huang et al., 2002].

Limitations in our study include lack of information

on individual risk factors for IHD other than BMI and

smoking, and the use of a job-exposure matrix to estimate

miners’ exposures, rather than direct individual measurements. Another limitation is lack of information on employment or exposure following study enrollment, which

resulted in some degree of exposure misclassification.

However, the largest part of the miners’ exposure occurred

prior to the study start, before implementation of the dust

control regulations under the Federal Coal Mine Health

and Safety Act of 1969 [U.S. Congress, 1969], which led

to lower dust levels in coal mines.

We were unable to assess the effect of silica exposure,

which has been found to be associated with an increased

risk of IHD in a surveillance study of silica exposed workers in other industries [Weiner et al., 2007]. Exposure to

silica from quartz dust generated during the mining process may contribute to miners’ IHD risk, particularly in

the Appalachian region, where a considerable amount of

rock may be cut in order to access coal deposits [Laney

et al., 2009].

Exposure to diesel emissions could also affect risk of

IHD among underground coal miners; however, diesel

equipment was not used extensively during the years of

the study. The use of diesel engines was prohibited in

Pennsylvania and West Virginia underground mines until

after the study’s end. Diesel equipment was used to a limited extent in the Midwest and South, and more frequently

in the West, a region which had a lower risk of IHD in

this study. Overall, any effect of diesel particulate exposure on study estimates of the effect of coal dust exposure

on IHD mortality should be small.

In conclusion, we found an increased risk of mortality

from IHD associated with cumulative exposure to coal

dust in this cohort. Mortality risk varied by coal region,

which may be due to regional variations in the composition of the coal mine dust particulate. The association of

increased risk of IHD with cumulative particulate exposure is consistent with air pollution studies, which have

shown that long-term cumulative exposures to particulate

are strongly related to IHD mortality [Schwartz et al.,

2008; Pope et al., 2009].

REFERENCES

Attfield MD, Kuempel ED. 2008. Mortality among U.S. underground

coal miners: A 23-year follow-up. Am J Ind Med 51:231–245.

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.

Attfield MD, Seixas NS. 1995. Prevalence of pneumoconiosis and

its relationship to dust exposure in a cohort of U.S. bituminous coalminers and ex-miners. Am J Ind Med 27:137–151.

Atuhaire LK, Campbell MJ, Cochrane AL, Jones M, Moore F. 1986.

Specific causes of death in miners and ex-miners of the Rhondda

Fach 1950-80. Br J Ind Med 43:497–499.

Christie DG, Brown AM, Taylor RJ, Seccombe MA, Coates MS.

1995. Mortality in the New South Wales coal industry, 1973–1992.

Med J Aust 163:19–21.

Coal Utilization. 2011. In Encyclopædia Britannica. http://www.

britannica.com/EBchecked/topic/122944/ utilization Accessed April

6, 2011.

Costello J, Ortmeyer CE, Morgan WK. 1975. Mortality from heart

disease in coal miners. Chest 67:417–421.

David HA, Moeschberger ML. 1978. The theory of competing risks.

Griffin’s statistical monographs and courses no. 39. New York, NY:

Macmillan Pub. Co., Inc.

Dockery DW, Pope CA, Xu X, Spengler JD, Ware JH, Fay ME,

Ferris BG, Speizer FE. 1993. An association between air pollution

and mortality in six U.S. cities. N Engl J Med 329:1753–1759.

EPA. 2006. National Ambient Air Quality. Standards for Particulate

Matter. Final Rule. 40 CFR Part 50. In: Agency USEP editor.

Fine JP, Gray RJ. 1999. A proportional hazards model for the subdistribution of a competing risk. J Am Stat Assoc 94:496–509.

Fox AJ, Collier PF. 1976. Low mortality rates in industrial cohort

studies due to selection for work and survival in the industry. Br J

Prev Soc Med 30:225–230.

Franklin M, Koutrakis P, Schwartz P. 2008. The role of particle composition on the association between PM2.5 and mortality. Epidemiology 19:680–689.

Gilbert ES. 1982. Some confounding factors in the study of mortality

and occupational exposures. Am J Epidemiol 116:177–188.
7

Grambauer N, Schumacher M, Beyersmann J. 2010. Proportional

subdistribution hazards modeling offers a summary analysis, even if

misspecified. Stat Med 29:875–884.

Gray B. 2010. Subdistribution Analysis of Competing Risks. R package cmprsk, version 2. 2-1. http://cran.r-project.org/web/packages/

cmprsk/index.html Accessed April 6, 2011.

Huang C, Li J, Zhang Q, Huang X. 2002. Role of bioavailable iron

in coal dust-induced activation of activator protein-1 and nuclear factor of activated T cells: Difference between Pennsylvania and Utah

coal dusts. Am J Respir Cell Mol Biol 27:568–574.

Kan H, London SJ, Chen G, Zhang Y, Song G, Zhao N, Jiang

L, Chen B. 2007. Differentiating the effects of fine and coarse

particles on daily mortality in Shanghai. China Environ Int 33:376–

384.

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.

Laden F, Neas LM, Dockery DW, Schwartz J. 2000. Association of

fine particulate matter from different sources with daily mortality in

six U.S. cities. Environ Health Perspect 108:941–947.

Laney AS, Petsonk EL, Attfield MD. 2009. Pneumoconiosis among

underground bituminous coal miners in the United States: Is silicosis

becoming more frequent? Occup Environ Med 67:652–656.

Lau B, Cole SR, Gange SJ. 2009. Competing risk regression models

for epidemiologic data. Am J Epidemiol 170:244–256.

Liddell FD. 1973. Mortality of British coal miners in 1961. Br J Ind

Med 30:15–24.

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.

Miller BG, MacCalman L. 2010. Cause-specific mortality in British

coal workers and exposure to respirable dust and quartz. Occup

Environ Med 67:270–276.

Morgan WK, Burgess DB, Jacobson G, O’Brien RJ, Pendergrass

EP, Reger RB, Shoub EP. 1973. The prevalence of coal workers’

pneumoconiosis in US coal miners. Arch Environ Health 27:221–

226.

Ostro B, Broadwin R, Green S, Feng WY, Lipsett M. 2006. Fine

particulate air pollution and mortality in nine California counties:

Results from CALFINE. Environ Health Perspect 114:29–33.

Ostro BD, Feng WY, Broadwin R, Malig BJ, Green RS, Lipsett MJ.

2008. The impact of components of fine particulate matter on cardiovascular mortality in susceptible subpopulations. Occup Environ

Med 65:750–756.

Ozkaynak H, Thurston GD. 1987. Associations between 1980 U.S.

mortality rates and alternative measures of airborne particle concentration. Risk Anal 7:449–461.

Page SJ, Organiscak JA. 2000. Suggestion of a cause-and-effect relationship among coal rank, airborne dust, and incidence of workers’

pneumoconiosis. Am Ind Hyg Assoc J 61:785–787.

Pepe MS, Mori M. 1993. Kaplan–Meier, marginal or conditional

probability curves in summarizing competing risks failure time data.

Stat Med 12:737–751.

Pintilie M. 2006. Compteting risks: A practical perspective.

Hoboken, NJ: John Wiley and Sons.

Pope CA III, Dockery DW. 2006. Health effects of fine particulate

air pollution: Lines that connect. J Air Waste Manage Assoc 56:709–

742.

Pope CA, Burnett RT, Thurston GD, Thun MJ, Calle EE, Krewski D,

Godleski JJ. 2004. Cardiovascular mortality and long-term exposure

to particulate air pollution: Epidemiological evidence of general

pathophysiological pathways of disease. Circulation 109:71–77.

Pope CA III, Ezzati M, Dockery DW. 2009. Fine-particulate air

pollution and life expectancy in the United States. N Engl J Med

360:376–386.

Puett RC, Schwartz J, Hart JE, Yanosky JD, Speizer FE, Suh H,

Paciorek CJ, Neas LM, Laden F. 2008. Chronic particulate exposure,

mortality, and coronary heart disease in the nurses’ health study 1.

Am J Epidemiol 168:1161–1168.

R Development Core Team. 2011. R: A language and environment

for statistical computing. Vienna, Austria: R Foundation for Statistical Computing. http://www.R-project.org Accessed March 30, 2011.

Rockette HE. 1977. Cause specific mortality of coal miners. J Occup

Med 19:795–801.

Schlick DP. 1971. Respirable Coal Mine Dust Standards and Their

Enforcement under the Coal Mine Health and Safety Act of 1969.

Inhaled Particles III, vol 2. Old Woking, Surrey, United Kingdom:

Unwin Brothers. p 1007–1013 .

Schwartz J. 1999. Air pollution and hospital admissions for heart

disease in eight U.S. counties. Epidemiology 10:17–22.

Schwartz J. 2001. Air pollution and blood markers of cardiovascular

risk. Environ Health Perspect 109 (Suppl 3): 405–409.

Schwartz J, Dockery DW, Neas LM. 1996. Is daily mortality associated specifically with fine particles? J Air Waste Manage Assoc

46:927–939.

Schwartz J, Coull B, Laden F, Ryan L. 2008. The effect of dose and

timing of dose on the association between airborne particles and survival. Environ Health Perspect 116:64–69.

Seixas NS, Robins TG, Rice CH, Moulton LH. 1990. Assessment of

potential biases in the application of MSHA respirable coal mine

dust data to an epidemiologic study 13. Am Ind Hyg Assoc J

51:534–540.

Stayner L, Steenland K, Dosemeci M, Hertz-Picciotto I. 2003. Attenuation of exposure-response curves in occupational cohort studies at

high exposure levels. Scand J Work Environ Health 29:317–324.

U.S. Congress. 1969. Federal Coal Mine Health and Safety Act of

1969 (Public Law 91-173).

Une H, Esaki H, Osajima K, Ikui H, Kodama K, Hatada K. 1995. A

prospective study on mortality among Japanese coal miners. Ind

Health 33:67–76.

Vermylen J, Nemmar A, Nemery B, Hoylaerts MF. 2005. Ambient

air pollution and acute myocardial infarction. J Thromb Haemost

3:1955–1961.

Weiner J, Barlow L, Sjogren B. 2007. Ischemic heart disease mortality among miners and other potentially silica-exposed workers. Am J

IndMed 50:403–408.