pneumonconiosis due to coal

1. PNEUMOCONIOSIS
COAL
MS/OOO38/014
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2. 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
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3. 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 decades following exposure to these dusts
• The mineral dust pneumoconioses by- coal dust, silica, and
asbestos
Silica – silicosis
Asbestos –asbestosis
Coal – simple CWP and complicated CWP (PMF)
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4. Coal Mine Dust Lung Disease
caused by inhalation of coal mine dust and the body’s reaction to it
1. Fibrotic diseases – damage/destroy lung tissue
– Coal workers' pneumoconiosis “CWP”
– Silicosis
– Mixed dust pneumoconiosis
– Dust-related diffuse fibrosis
2. Airflow diseases – block movement of air
– Bronchitis
– Emphysema
– Mineral dust small airway disease “COPD”
3. Infectious diseases – dust reduces immunity
– Tuberculosis/related
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5. 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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6. 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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7. Anthracosis (urban dwellers)
morphology
• Gross Streaks of anthracotic pigment in lymphatics and
draining hilar lymph nodes
Microscopy
• Carbon pigment in alveolar and interstitial macrophages, in
connective tissue and lymphatics and lung hilus.
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8. 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
• engulfed by alveolar and interstitial macrophages,
phagocytize coal particles, transport them up the
mucociliary elevator to be expelled in the mucus or through
the interstitial lymphatic clearance route – this the
physiologic pathway.
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9. Pathogenesis cont’d
• The lungs are exposed to dust particles larger than 2-5 µm
in diameter for a significant period;
• The dust-laden macrophages accumulate in 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 deposited along the
vascular tree, compromising the vessels and ensuing ischemic
necrosis.
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10. Pathogenesis cont’d
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11. 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 lesions are 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, rounded opacities in the outer thirds of the lung
fields and the mid and upper zones.
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12. 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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13. Simple CWP - Gross Morphology
GROSS HISTOLOGICAL
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14. 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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15. 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 and pigment with the center of the
lesions being necrotic Associated with pulmonary hypertension
and corpulmonale
• . PMF appears as rounded, sausage-shaped or ovoid opacities
greater than 1 cm in diameter, which are well demarcated
from the adjacent lung and may vanish if the contents are
expectorated
• 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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16. PMF - Morphology
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17. Caplan’s syndrome
- 1st 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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18. Diagnosis - CWP
• A full and detailed medical, occupational and environmental
history is taken followed by Physical examination, with a
focus on the chest area
• Imaging procedures, such as chest X-rays and Computed
Tomography (CT) scans, remain the primary diagnostic
tools used 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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19. Diagnosis cont’d
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20. Chest radiograph
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21. The ILO 2011 classification system
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22. 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 culture can 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
• Bronchoscopy with a lung biopsy, an invasive technique that involves the
removal of a small piece of lung tissue to be examined in the laboratory
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23. Tuesday, February 21, 2017 23

24. 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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25. PROGNOSIS
• Other constitutional symptoms such as fever and night
sweats may occur if a superimposed mycobacterial infection
is present
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26. Prevention, Treatment and
Management
• Preventing exposure to coal dust prevents disease.
• This is important, as no effective treatments for CWP exist.
• The effects of 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 preventive methods.
• Chest radiographs are serially monitored in 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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27. References
• Robbins Basic Pathology 9th 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
perspective pdf 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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28. Thank you!
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