coal worker pnemoconiosis,silicosis

1. OCCUPATIONAL LUNG DISEASES

2. Dust Deposition and Lymphatic
Clearance:
 deposition of particles 1–5 µm in
diameter in and around the
respiratory bronchioles-
centrilobular location
 Perilymphatic disease
subpleural,peribronchovascular or
along lobular septae.
 Posterosuperior segment predilection of
dust retention.

3. PNEUMOCONIOSIS CLASSIFICATION
ACCORDING TO ILO (INTERNATIONAL LABOUR OFFICE)
TYPE OF OPACITIES
Silicosis,
coal worker's pneumoconiosis
nodular opacities:
p = <1.5 mm
q = 1.5-3 mm
r = 3-10 mm
 Asbestosis
 linear opacities:
 s = fine
 t = medium
 u = coarse/blotchy
 PROFUSION/SEVERITY
 0 = normal
 1 = slight
 2 = moderate
 3 = advanced

4. Induction Periods
 Short:
 Asthma
 Infections
 Allergic alveolitis
 Toxic poisonings
 Long:
 Pneumoconioses
 Neoplasms

5. acute reactions chronic reactions
inflammation and edema fibrosis or granuloma
1.Upper Respiratory Tract Irritation
Occupational Rhinitis
2.Airway Disorders
Occupational Asthma
Reactive Airways Dysfunction
(Byssinosis)
3.Inhalation injury
Hypersensitivity Pneumonitis
4.Pleural Disease
Pleural effusions and pleuritis
(Asbestos)
1.Interstitial Fibrosing Diseases
Asbestosis (non-malignant
pulmonary disease)
Silicosis
Coal Workers’Pneumoconioses
Berylliosis
Chronic Bronchitis and Chronic
Airways Disease
2.Malignancies
Malignant Mesothelioma
Lung Cancer
Laryngeal Cancer
Sinonasal Cancer

6. CLASSIFIED
fibrotic
( focal nodular ,diffuse fibrosis)
nonfibrotic
(particle-laden
macrophages,
no fibrosis )1.silicosis -Nodular fibrosis
2.coal worker pneumoconiosis-
Macule formation with focal
emphysema
3.asbestosis --Diffuse fibrosis
4.berylliosis- Granulomatous reaction
5.talcosis
1.siderosis
2.stannosis
3.baritosis

7. Silicosis
 principal sources- free silica in mining, quarrying,
and tunneling.
 fine crystalline silicon dioxide Inhalation
 Silica particles- breakdown of macrophage releases
enzymes –progressive fibrogenic response even
after cessation of dust exposure.

8. Silicosis
 small, well-circumscribed nodules that are 2–5 mm
in dia, mainly inv upper & posterior lung zones.
 GGO
 20% calcify centrally
 Lymphadenopathy is common
 Eggshell calcification of hilar nodes (5%)
DDx: Sarcoidosis

10. SILICOSIS
 2 clinical forms:
 Acute silicosis (alveolar silicoproteinosis)
 classic silicosis (chr interstitial reticulonodular disease)
simple complicated
 OBSTRUCTIVE LUNG DISEASE
 LUNG CANCER
 Silicotuberculosis

11. Acute Silicosis
 Rare
 heavy exposure to free
silica-in closed spaces for
6–8 months.
 rapidly progressive, with
death caused by
respiratory failure.
 HRCT - "crazy paving"
pattern
 No silicotic nodules.
 DD-Alveolar proteinosis
(silicoproteinosis)

12. bilateral consolidation ,
GGO in perihilar region
“central bat-wing consolidation .”

13. CHRONIC SIMPLE SILICOSIS
 10--20 years of dust exposure
 Rt upper lobes--posterior lung zones
 nodules are in perilymphatic distribution
 centered along the bronchovascular bundles,
centriacinar portion of the lobule, & in the
subpleural lung, where the nodules form these
pseudoplaques.

14.  1-10mm well defined rounded opacities 
centrilobular & peribronchial;
 nodules surrounded by focal emphysema (focal dust
emphysema)
 calcify
 hilar + mediastinal lymphadenopathy, may calcify in 5%
(eggshell pattern)

15. Simple silicosis
pseudoplaques
diffuse nodular opacities with
relative sparing of the basal lung
zones
HRCT shows numerous small nodules

16. Complicated Silicosis (PROGRESSIVE MASSIVE FIBROSIS)
large opacities >1 cm in diameter
mid zone /periphery of upper lung migrating toward hila
 Relatively bilateral symmetric + nonsegmental
conglomerate sausage-shaped masses with ill-defined
margins (in advanced stages)
compensatory emphysema in unaffected portion between
mass + pleura
slow change over years
may calcify + cavitate (ischemic necrosis/TB)

18. CXR-large b/l opacities in the upper zones of the lung, as well as upward
elevation of both hila.
CT-shows bilateral conglomerate masses with calcifications, findings that
represent PMF in the upper zone of both lungs.

19. OBSTRUCTIVE LUNG DISEASE AND LUNG CANCER
chronic bronchitis, & Emphysema.
Tobacco smoking may cause an additive effect.
Silicotuberculosis
synergistic relationship between silicosis + tuberculosis

20. COAL WORKER PNEUMOCONIOSIS

21. CWP
 Simple CWP- asymptomatic & is often a radiographic
diagnosis.
 Progressive massive fibrosis (PMF) can occur more
frequently with exposure to silica.
 CXR- small nodules predominantly in upper & posterior
zone. Hilar lymph node enlargement is not uncommon
 eggshell calcification does not generally occur.
 usually bilateral, progressive, and may cavitate or
become calcified.
 DD--tumors, tuberculosis scars, or Caplan’s nodules

22. 22
CAPLANS SYNDROME
 coal workers with rheumatoid disease may develop
nodules even after relatively low exposures to
dust.
 The lesions are typically subpleural.
 The lesions may grow rapidly,appear in crops(in
contrast to silicotic/CWP nodules that appears over
a period of time)cavitate and produce a
pneumothorax

23. 23

24. 24
Differentiate PMF from lung cancer
 Clinically and radiologically important
 bilateral occurrence : DDx with tumors or
tuberculosis
 Unilateral masses occur : DDx is difficult
 Chest PA
 Shape of mass
 Calcification
 Satellite Nodules
 Course of PMF

25. 25
Differentiate from lung
cancer
 Shape of mass
 typically in periphery of lung
 smooth, sharp, elongated lateral border parallel rib
cage
 projected 1~3 cm from lateral costal margin
 medial border : ill-defined vs. lateral : sharp
 tends to be thin, carcinomas tend to be spherical
 Calcification
 thick eggshells -> exclude primary lung cancer
 central dot calcification,
  Linear calcifications ; not in cancer

26. 26
Differentiate from lung
cancer
 Satellite Nodules
 multiple small nodules near a lung mass in
pneumoconiosis or infection
 rare in carcinoma
 Course of PMF
 mass formed by coalescence of nodule, rather than
by growth of a single nodule
 mass has decreased in size

27. 27
Differentiate from lung
cancer
# MR imaging : useful
★ lung cancer vs PMF
 High SI on T2WI vs low SI T1WI, T2WI
 Low SI on T2WI MR images -> PMF
# PET
 Intensive uptake of FDG in PMF
 Observation of resultant mass enhancement on images
-> confusion of PMF with lung cancer
 Histopathologic analysis should be performed

28. Progressive massive fibrosis
(a)HRCT scans --irregularly marginated 20–30mm nodules accompanied by smaller satellite
nodules and surrounding reticulation in the upper lobe of both lungs.
(b) T1-w image - slightly hyperintense lesions in both upper lobes.
(c) T2-w image -absence of signal at the lesion sites and a small pleural effusion in the rt lung.
(d) PET-CT scan -increased uptake of FDG in both nodules and in a right paratracheal LN.

29. Lung cancer and coal worker pneumoconiosis
(a) HRCT- welldefined 2-cm-diameter nodule in an upper segment of the lower
lobe of the left lung, a finding that represents a combined neuroendocrine large
cell carcinoma and adenocarcinoma, as well as multiple smaller nodules
(b) T2-weighted -high-signal-intensity nodule in the lower lobe.
(c) (PET)-CT scan - a high uptake of FDG in the nodule, suggestive of malignancy.
(d) gross specimen- left lower lobectomy shows the cancer (arrow) and multiple
black-pigmented nodules (arrowheads)In the lung parechyma and pleural surface

30.  refers to pulmonary fibrosis secondary to asbestos exp.
 Risk factors: Longer (approx. 20 years) exposure to the
amphibole fiber type.
 not associated with smoking
 Two large groups:
serpentines (Chrysotile)and amphiboles(crocidolite).
Asbestosis

31.  2 major sources of asbestos dust:
(a) the primary occupations in asbestos mining.
(b) secondary occupations --insulation manufacturing, textile
manufacturing, construction, shipbuilding, and the
manufacture and repair of gaskets and brake linings.
 Asymptomatic until 20 years after initial exposure.
 Long asbestos fiber (up to 100 µm in length), penetrates
deeply into the lung and pleura, and has a fibrogenic effec
on respiratory bronchioles, alveoli, and pleura.

32. Asbestos-related diseases
Benign
Pleural diseases
1.plaques
2.diffuse pleural thickening
3.effusion
4.calcification
Parenchymal diseases
1.Asbestosis [parenchymal
fibrosis caused by asbestos
inhalation]
2.Rounded atelectasis
3.Benign fibrotic masses
4.Transpulmonary bands
Malignancy
1.Malignant mesothelioma
2.Bronchogenic carcinoma

33. FOCAL PLEURAL PLAQUES (65%):
Incidence: most common manifestation of
exposure
 Location: bilateral + multifocal; following rib
contours;
Site: parietal pleura (visceral pleura typically spared)
Plaques are often holly leafed shaped
Apices + costophrenic angles typically spared.

34. DIFFUSE PLEURAL THICKENING :
smooth uninterrupted diffuse thickening of parietal
pleura extending over at least 1/4 of chest wall
(visceral pleura involved in 90%, but difficult to
demonstrate)
 smooth; difficult to assess when viewed en face
 Usually involves the costophrenic angles
 May be associated with rounded atelectasis
DDx: pleural thickening from parapneumonic
effusion, hemothorax, connective tissue disease

35. pleural plaques
right side∕
rounded
atelectasis
diffuse pleural thickening
Diaphragmatic pleural plaques

36. visceral pleural plaque in
the right major fissure &
curvilinear bands of
hyperattenuation in the
posterior subpleural area.
calcified pleural plaques
hallmark of asbestos
exposure.

37. 37
PLEURAL CALCIFICATION:
HALLMARK of asbestos exposure!
detected by radiography in 25%, by CT in 60%
Histo: calcification starts in parietal pleura; calcium
deposits may form within center of plaques
Dense lines paralleling the chest wall, mediastinum,
pericardium, diaphragm
 Bilateral diaphragmatic calcifications with clear
costophrenic angles are PATHOGNOMONIC
advanced calcifications are leaflike with thick-rolled edges
DDx: talc exposure, hemothorax, empyema, therapeutic
pneumothorax for TB (often unilateral, extensive sheet like
on visceral pleura)

38. Pleural effusion
 earliest manifestation -within 10 years of exposure,
 usually transient but requires close follow-up .

39. Asbestosis
 Parenchymal fibrosis begins in and around the respiratory
bronchioles in the lower lobes adjacent to the visceral pleura
 progress to diffuse interstitial fibrosis and "honeycombing," with
complete destruction of the alveolar architecture.
 Asbestos bodies- observed microscopically in bronchoalveolar
lavage fluid or tissue section .
 It may remain static or progress over time.

40. Radiologic changes consist of
 small, irregular opacities or linear hyperattenuating
areas
fine reticulations
coarse linear pattern with honeycombing.
 most severe in the posterior subpleural lower
lungs.

41. RETICULAR
INFILTRATES

42. HONEYCOMB LUNG

43. Prone HRCT scan –b/l
subpleural reticular
hyperattenuating areas,
small cysts, traction
bronchiectasis, & GGO.

44. 44
ASBESTOSIS VS IPF
FAVORS ASBESTOSIS
 Pleural plaques
 Subpleural branching opacities
 Subpleural curvilinear lines
 Parenchymal bands
 Homogeneous subpleural opacities

45. o Pleural plaques
o Sub pleural curvilinear lines
o Parenchymal bands
 Traction bronchectasis
 Bronchiloectasis
 honeycombing
ASBESTOSIS IPF

46. ATELECTATIC ASBESTOS PSEUDOTUMOR/ ROUND
ATELECTASIS/ FOLDED LUNG
 In folding of redundant pleura + segmental/subsegmental
atelectasis
 b/l posterobasal, 2.5-8 cm focal subpleural mass abutting a
region of thickened pleura
CT: rounded/lentiform shaped
peripheral mass abutting pleura
pleural thickening ± calcification
curving of pulmonary vessels and bronchioles into edge of
lesion (vacuum cleaner/comet tail sign )
volume loss of affected lobe
 crow's feet = linear bands radiating from mass into lung

47. Comet
tail sign

48. PARENCHYMAL BAND “CROWS FEET”

49. 49
LUNG CANCER In those with asbestosis, the cancer is more likely to
arise in the lower lobes in contrast to general smokers.
Associations with lung cancer and mesothelioma
Asbestos-related lung cancer is usually either squamous
cell or adenocarcinoma
 Bronchogenic carcinoma is almost always associated
with cigarette smoking
Mesotheliomas are not related to cigarette smoking
Mesotheliomas most often due to crocidolite particles

50. 50
Mesothelioma
 Mesothelioma is a rare pleural malignancy seen with
asbestos exposure.
 The majority have no plaques. Long thin fibers are more
likely to induce mesothelioma, thus crocidolite is more
neoplastic than chrysotile.
 The hemithorax is usually small, pleural effusion is nearly
universal.
 Prognosis is poor, 12 month median survival.

51. Mesothelioma
 Rare.
 majority have no plaques.
crocidolite is more neoplastic
than chrysotile.
 small, pleural effusion
 poor Prognosis.

52. Malignant mesothelioma
• both parietal and visceral
pleura mass.Local invasion is
common
•CXR -Ipsilateral effusion to
the pleural disease &
contralateral pleural plaques
•diagnosed by Open biopsy .

53. Mesothelioma indicated by
the central pleural effusion

54. Byssinosis in a 56-year-old woman who had
had frequent episodes of “Monday fever”
and dyspnea while working in a cotton
factory over a 7-year period. (a) Chest
radiograph shows diffuse, ill-defined
haziness, predominantly in the lower lung
zones. (b) High-resolution CT scan shows
numerous ill-defined small nodules with
ground-glass attenuation in both lungs.

55. Mercury vapor poisoning in a 34-year-
old woman worked for a
mercurythermometer manufacturer for
30 months. presented with headache
and dyspnea and suffered from
chronicgingivitis.Chestxray showed
perivascular haziness and fine reticular
opacities in the parahilar area of both
lungs. CT scan shows areas of ground-
glass attenuation, poorly defined
centrilobular nodules (arrows), and
bronchial wall thickening. Note the
relative sparing of the periphery of
both lungs.

56. Occupational Lung Cancers
 Asbestos
 Arsenic
 Bischloromethyl ether
 Coke oven fumes
 Insoluble Hexavalent
chromium cmpds
 Soluble nickel
 Mustard gas
 Radon daughters
asbestosis lower lobes cancer is more likely-squamous cell or
adenocarcinoma
 Bronchogenic carcinoma is almost always associated with
cigarette smoking

57. SIDEROSIS
 inert iron oxide/metallic iron deposits
 diffuse fine reticulonodular opacities (may disappear after
exposure discontinued)
 small round opacities (indistinguishable from silica/coal)
NO secondary fibrosis + NO hilar adenopathy
HRCT:--widespread poorly defined centrilobular micronodules
 branching linear structures
 extensive ground-glass attenuation without zonal
predominance

58. BERYLLIUM-INDUCED LUNG DISEASE
 extremely light metal Beryllium with a high modulus of
elasticity (stiffness).
 chronic beryllium disease (CBD or berylliosis)-
delayed-type hypersensitivity reaction -granulomatous lung
disease similar to sarcoidosis.
 Lung primarily affected.
 Other sites -extrapulmonary lymph nodes, skin, salivary
glands, liver, spleen, kidney, bone, myocardium, and skeletal
muscle.
 usually nonspecific Symptoms – later--Dyspnea -mc symptom.

59.  XRAY chest -50%
patients normal.
Abnormal findings -
hilar
adenopathy,increas
ed interstitial
markings.
HRCT:GGO,parenchy
mal nodules,septal
lines.

60.  The diagnosis of CBD is based on the presence of:
History of beryllium exposure
positive blood or bronchoalveolar lavage
beryllium-specific lymphocyte proliferation test
presence of non-necrotizing granuloma on lung bx
25% may show negative results

61. CONCLUSION
SILICOSIS--multiple small rounded opacities in upper lobes
5% Eggshell calcification of hilar nodes.
Asbestosis--Pleural without parenchymal disease.
 B/l Parietal pleural plaques in the mid lung –mc.
 50% Pleural calcification.

62. thank you