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2 figures, 2 tables omitted
Pneumoconioses are caused by the inhalation and deposition of mineral
dusts in the lungs, resulting in pulmonary fibrosis and other parenchymal
changes. Many persons with early pneumoconiosis are asymptomatic, but advanced
disease often is accompanied by disability and premature death. Known pneumoconioses
include coal workers' pneumoconiosis (CWP), silicosis, asbestosis, mixed dust
pneumoconiosis, graphitosis, and talcosis. No effective treatment for these
diseases is available.1 This report describes
the temporal patterns of pneumoconiosis mortality during 1968-2000, which
indicates an overall decrease in pneumoconiosis mortality. However, asbestosis
increased steadily and is now the most frequently recorded pneumoconiosis
on death certificates. Increased awareness of this trend is needed among health-care
providers, employers, workers, and public health agencies.
The National Institute for Occupational Safety and Health (NIOSH) maintains
a mortality surveillance system for respiratory diseases of occupational interest.2 The data are drawn from annual National Center
for Health Statistics (NCHS) multiple-cause-of-death mortality files, which
include all deaths in the United States since 1968. For this report, pneumoconiosis
deaths were identified during 1968-2000, the most recent year for which complete
data are available, and include any death certificates for which an International Classification of Diseases (ICD) code* for
CWP, silicosis, asbestosis, or unspecified/other pneumoconiosis was listed
as either the underlying or contributing cause of death. Age-adjusted death
rates (per million population per year) for periods of interest were calculated
by using the mid-year population as a denominator. Age standardization was
performed by using the 2000 U.S. Census population.
During 1968-2000, pneumoconiosis was recorded on 124,846 death certificates.
Comparing 1968-1981 with 1982-2000, death rates among males declined 36% for
CWP and approximately 70% for both silicosis and unspecified/other pneumoconiosis,
but increased nearly 400% for asbestosis. For both sexes, the decline was
smaller among non-Hispanic blacks (26%) than among non-Hispanic whites (40%)
for CWP but similar or greater for silicosis and unspecified/other pneumoconiosis,
whereas the death rates for asbestosis increased 448% among blacks versus
342% among whites. Death rates among females were substantially lower than
among males and, except for asbestosis, indicated decreases among both non-Hispanic
whites and blacks. Asbestosis death rates increased among those aged ≥45
years; otherwise, death rates for the various pneumoconioses decreased regardless
of age category.
The number of asbestosis deaths increased from 77 deaths (annual age-adjusted
death rate: 0.54 per million population) in 1968 to 1,493 deaths (6.88 per
million) in 2000; deaths for all other pneumoconioses decreased. CWP was the
most frequently recorded pneumoconiosis from 1968 until 1998, when it was
surpassed by asbestosis. Silicosis mortality declined steadily and, since
1993, was the least recorded category of pneumoconiosis. The geographic distributions
of mortality for each type of pneumoconiosis for the 1968-1981 and 1982-2000
periods indicate that asbestosis increased substantially throughout the United
States, particularly in the coastal states, where asbestos was used frequently
in shipbuilding (Figure 2); CWP and the other pneumoconioses, which tend to
occur in the mining and industrial regions of the country, had either little
change or a decline during the two study periods.
Information from death certificates regarding usual occupation and industry
was available for deaths in selected states only for 1985-1999.2 During
this period, ship and boat building/repairing was replaced by nonmetallic
mineral/stone products as the industry with the highest proportionate mortality
ratio (PMR) for asbestosis. In addition, explosives worker replaced mining
machine operators as those whose occupation had the highest PMR for other/unspecified
MD Attfield, PhD, JM Wood, MS, National Institute for Occupational Safety
and Health; VC Antao, MD, GA Pinheiro, MD, EIS officers, CDC.
The decline in overall pneumoconiosis mortality is attributed to reductions
in CWP, silicosis, and other/unspecified pneumoconiosis mortality. The overall
decline in CWP mortality follows the general reduction in the coal mining
workforce since the 1920s. The Federal Coal Mine Health and Safety Act of
1969 introduced lower dust limits in the mining environment to protect the
health of the nation's coal miners.3 Resulting
lower dust levels have contributed to major reductions in disease among actively
employed coal miners4; however, the full
impact of dust control on CWP mortality is not yet known. As with coal mining,
the number of workers exposed to hazardous silica dust has declined through
the loss of jobs in heavy industry. In addition, dust limits for silica in
the United States also have been reduced steadily for approximately 30 years.5 Both job losses and reductions in exposures have
contributed to the decline in silicosis mortality.
Asbestosis is the only major pneumoconiosis to demonstrate increased
mortality. Because asbestosis mortality peaks 40-45 years after initial occupational
exposure to asbestos,6 this upward trend
reflects past exposure to asbestos fibers. Asbestos consumption increased
substantially during and after World War II, with a peak in 1975 followed
by a steep decrease beginning in the 1980s.7 Given
the temporal pattern of usage and latency and survival considerations, asbestosis-related
mortality is expected to increase for at least another decade. Asbestos-containing
materials that continue to be used in some workplaces and remain in buildings
represent a potential risk.
The findings in this report are subject to at least five limitations.
First, occupation and industry codes that meet NCHS quality criteria are available
only for certain states and for certain years. Thus, PMRs only reflect the
industrial and occupational profiles of those states in those years. Second,
these codes represent only the usual industry and occupation as entered on
each death certificate, which is not always the industry and occupation in
which the decedent's causative exposure occurred. Third, the state of residence
at death is not always the state in which the decedent's causative exposure
occurred, especially given the typically long latency and chronic course of
the pneumoconioses. Fourth, slight differences exist in the ICD coding for
asbestosis between the 9th and 10th revisions. In the 10th revision, the rubric
for code J61 is "pneumoconiosis due to asbestos and other mineral fibers,"
whereas the rubric for the 8th and 9th revisions was simply "asbestosis."
The overall effect of this change is unclear but might have resulted in an
increase in the number of cases between the 9th and 10th revisions (i.e.,
between 1998 and 1999). Because occupational fiber exposures were predominantly
to asbestos, the net effect of this change probably is small; the trend of
increasing asbestosis deaths indicates no evidence of any substantial change
during 1998-1999. Finally, as with any data based solely on death certificate
information, cause of death information is subject to potential errors associated
with disease diagnosis, recording, and coding. For example, this information
can be impacted by temporal changes in public and medical awareness and practice.
In the years after the Farmington, West Virginia, mine disaster in 1968, the
nation's attention focused on hardships suffered by coal miners, with a possible
attendant rise in recording of CWP on death certificates. More recently, focus
on asbestosis has increased, with a marked increase in asbestos-related litigation.8 This trend also has raised awareness of asbestosis,
likely leading to its more frequent diagnosis and recording on death certificates.
In addition, new technologies such as computed tomography are used increasingly,
resulting in increased diagnostic sensitivity for pneumoconiotic diseases.
Despite these limitations, the national mortality data offer substantial
benefits: they are national in scope, well documented, and readily available.
These data are used to provide historical perspective on pneumoconiosis mortality
and, given sufficient time lag, can be used to assess the effectiveness of
preventive measures. They also can provide useful information on pneumoconiosis
by location, industry, and occupation, suggesting ways in which to target
preventive intervention and disease-management resources.
Considerable progress has been made toward elimination of the pneumoconioses.
Nevertheless, certain pneumoconioses considered to be nearly eliminated are
still occurring and causing deaths, even among young workers in the United
are preventable, and efforts to eliminate these diseases should continue.
This report is based on contributions by G Syamlal, MPH, C Philips,
RM Castellan, MD, National Institute for Occupational Safety and Health, CDC.
*ICDA-8 (1968-1978), ICD-9 (1979-1998), and ICD-10 (1999-2000).2
Changing Patterns of Pneumoconiosis Mortality—United States, 1968-2000. JAMA. 2004;292(7):795–796. doi:10.1001/jama.292.7.795
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