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
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
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)
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)
17.
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
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
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.
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
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.
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
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 .
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.