PNEUMOCONIOSIS
COAL
MS/OOO38/014
Monday, May 22, 2017 1
OBJECTIVES
•To define pneumoconiosis and explain the
etiology
•To list the types of pneumoconiosis
•To describe the various morphologies of
pneumoconioses
•To outline the pathogenesis of the types of
pneumoconioses
•To outline the clinical manifestations of coal
pneumoconiosis
•To explain treatment prevention and control
of pneumoconiosis
Monday, May 22, 2017 2
Pneumoconioses
Etiology
•Pneumoconioses are a group of lung diseases
caused by inhalation and accumulation of inorganic
or organic particles of mineral dust in the lungs.
•is a “long latency” disease which typically develops
gradually over a number years to decades following
exposure to these dusts
•The mineral dust pneumoconioses by-coal dust,
silica, andasbestos
Silica –silicosis
Asbestos –asbestosis
Coal –simple CWP and complicated CWP (PMF)
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COAL WORKERS
PNEUMOCONIOSIS (CWP)
•Associated with coal mining industry
•Pneumoconiosis due to coal dust inhalation
•Coal –carbon, crystalline silica, variety of
trace metals
•Types of coal –peat, lignite,(brown
coal/immature coal) sub-bituminous,
bituminous(black) anthracite(shiny/mature)
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Classification
•Asymptomatic anthracosis (due to
anthracite –coal)
-pigment accumulates without a
perceptible cellular reaction
•According to the severity of the lung
scaring-two types:
1. simple (Simple CWP) -no
dysfunction
2. complicated CWP -(progressive
massive fibrosis PMF)
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The ILO 2011 classification
system
Monday, May 22, 2017 6
Simple CWP –Pathogenesis
•CWP occurs when the body’s natural mechanism
for defending against and processing inhaled
dust becomes overwhelmed and in consequence,
over reactive.
•Coal particles reach respiratory tract –terminal
bronchioles
•engulfedby alveolar and interstitial
macrophages, phagocytizecoal particles,
transportthem up the mucociliary elevator to
be expelledin the mucus or through the
interstitial lymphatic clearanceroute –this the
physiologic pathway.
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Pathogenesis cont’d
•The lungs are exposedto dust particles larger than
2-5 µm in diameter for a significant period;
•The dust-laden macrophages accumulatein the
alveoli, an immune response may be triggered;
Fibroblasts secrete reticulin and entrap the
macrophages.
•When these macrophages migrate up the lymphatic
vessels, the resultant interstitial fibrosis will cause
the arterioles to become strangulated. As more
macrophages die, more fibroblasts, reticulin and
collagen are depositedalong the vascular tree,
compromisingthe vessels and ensuing ischemic
necrosis.
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Pathogenesis cont’d
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Morphology -
Simple CWP
•characterized by coal macules (1-2mm) and
the somewhat larger coal nodule
•The coal macule consists of dust-laden
macrophages; small amounts of collagen fibers
arrayed in a delicate network.
•The lesionsare scattered throughout the lung,
(the upper lobes and upper zones of the lower
lobes are heavily involved). Centrilobular
emphysema can occur
•Simple” pneumoconiosis is characterized by
small, ill-defined, roundedopacities in the
outer thirds of the lung fields and the mid and
upper zones.
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Morphology cont’d
Microscopy:
•Carbon laden macrophages& delicate collagen
fibers. Adjacent to respiratory bronchioles initially
(where dust settles), later interstitium & alveoli.
•Dilatation of respiratory bronchioles –focal dust
emphysema
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Simple CWP -Gross
Morphology
•
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Complicated CWP
•Also known as the “black lung disease”
•Occurs on a background of simple CWP
•Coalescence of coal nodules
•A form of Progressive Massive Fibrosis (PMF)
•Generally requires many years to develop
•Disease can progress even if dust exposure
ceases.
•Associated with increased incidence of clinical
tuberculosis, chronic bronchitis and emphysema
and independent of smoking
•In isolation, PMF does not appear to increase
the risk of lung cancer
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Complicated CWP -
Morphology
•It is characterized by usually multiple, intensely
blackened scars larger than 2 cm, sometimes
up to 10 cm in greatest diameter. On
microscopic examination the lesions are seen to
consist of dense collagen with the center of
the lesions being necrotic Associated with
pulmonary hypertension and corpulmonale
•A fibrotic mass is formed by exuberant
fibroblast activity that tends to occur in the
upper lobes of the bilateral lungs, showing an
“angel’s wing” appearance on plain radiographs
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Monday, May 22, 2017 15
PMF -Morphology
Monday, May 22, 2017 16
Caplan’s syndrome
-1
st
described in coal workers, may be seen in other pneumoconiosis
-Caplan syndrome results when PMF is associated with rheumatoid
factor.
-?? Immunopathologic mechanism
-Rheumatoid arthritis (RA) + Rheumatoid nodules (Caplan nodules) in
the lung
-Rheumatoid arthritis + pneumoconioses
-Caplan’s nodule = necrosis surrounded by fibroblasts, monocytes and
collagen
-s/s RA > lung symptoms
-The Caplan nodules exhibit a central area of coal dust and necrotic
collagenous tissue lying in concentric rings and it is surrounded by an
area of neutrophils with palisading fibroblasts
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Diagnosis -CWP
•A full and detailed medical, occupationaland
environmental history is taken followed by
Physical examination, with a focus on the chest
area
•Imaging procedures, such as chest X-raysand
Computed Tomography (CT) scans, remain the
primary diagnostic toolsused to visualize the
nodules and lung scarring and to evaluate the
presence and progression of the disease. The
radiographs obtained are to be compared
against the standardized set of X-rays
developed by the International Labor
Organization (ILO) which reflects the amount
of retained coal in the lungs
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Diagnosis cont’d
Monday, May 22, 2017 19
Chest radiograph
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Other methods of diagnosis
•Use of pulmonary function tests (PFTs) (i.e.Spirometry) in order
to determine the severity of the impairment of lung function
•Measurement of arterial blood gases (ABGs)can be used to the
determine impairments between oxygen and carbon dioxide in
the alveoli
•CBC count and a sputum culturecan be performed, if needed, to
eliminate the possibility of other infective processes
•The 6-minute walk test (6MWT), a simple, additional test that
can be performed as a mean of quantifying possible lung
impairment due to CWP
•Bronchoscopywith a lung biopsy, an invasive technique that
involves the removal of a small piece of lung tissue to be
examined in the laboratory
Monday, May 22, 2017 21
Clinical picture and further
complications
•Individuals suffering from simple CWP usually
display:
Chronic cough and shortness of breath on exertion may be
reported, however usually due to industrial bronchitis or
smoking
Mild loss of lung function
•As CWP progresses to the more severe and
complicated form, PMF, symptoms as follows may
arise:
Tightness in the chest
Dyspnea
Chronic Cough with black sputum
Pulmonary dysfunction (i.e. pulmonary hypertension)
Right-sided heart failure due to lung dysfunction
Cyanosis
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PROGNOSIS
•Other constitutional symptoms such as
feverand night sweatsmay occur if a
superimposed mycobacterial infection is
present
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Prevention, Treatment and
Management
•Preventing exposure to coal dust prevents disease.
•This is important, as no effective treatments for
CWP exist.
•The effectsof simple and complicated CWP on the
lungs are irreversible. There is so no specific
treatment for the disease available so far, other
than palliative and preventivemethods.
•Chest radiographsare serially monitoredin order
to prevent further development of the disease
•As smoking can contribute to the condition, it is
strongly advised that the individual stops smoking.
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References
•Robbins Basic Pathology 9
th
Edition by Vinay Kumar, Abul K.
Abbas, Jon C. Aster
•Towards Understanding Coal Workers Pneumoconiosis pdf by
Alice Maria Ciobanu SID: 3395606
•Coal Workers Pneumoconiosis –‘An Old Disease That Is Still
Among Us’ pdf by Wayne T. Sanderson, PhD, CIH, Professor
and Chair University of Kentucky Annual Pilot Research
Project (PRP) Symposium University of Cincinnati.
•Clinical Focus, Coal workers’ pneumoconiosis, an Australian
perspectivepdf by Graeme R Zosky, Ryan F ,Elizabeth J
Silverstone, Fraser J Brims, Susan Miles, Anthony R Johnson,
Peter G, Deborah H
•(Rom and Markowitz; 2007)
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