OCCUPATIONAL LUNG DISEASES

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.

PNEUMOCONIOSIS CLASSIFICATION ACCORDING TO ILO (INTERNATIONAL LABOUR OFFICE) TYPE OF OPACITIES

Silicosis, coal worker's pneumoconiosis

nodular opacities:p = <1.5 mmq = 1.5-3 mmr = 3-10 mm

Asbestosis linear opacities:

s = fine t = medium u = coarse/blotchy

PROFUSION/SEVERITY 0 = normal 1 = slight 2 = moderate 3 = advanced

Induction PeriodsShort:

AsthmaInfections Allergic alveolitisToxic poisonings

Long:PneumoconiosesNeoplasms

acute reactions chronic reactions

inflammation and edema fibrosis or granuloma

1.Upper Respiratory Tract Irritation

Occupational Rhinitis2.Airway Disorders

Occupational AsthmaReactive Airways Dysfunction

(Byssinosis)3.Inhalation injury

Hypersensitivity Pneumonitis4.Pleural Disease

Pleural effusions and pleuritis (Asbestos)

1.Interstitial Fibrosing Diseases

Asbestosis (non-malignant pulmonary disease)

SilicosisCoal

Workers’PneumoconiosesBerylliosisChronic Bronchitis and

Chronic Airways Disease2.Malignancies

Malignant MesotheliomaLung CancerLaryngeal CancerSinonasal Cancer

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 fibrosis4.berylliosis- Granulomatous reaction5.talcosis

1.siderosis 2.stannosis 3.baritosis

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.

Silicosissmall, well-circumscribed nodules that are 2–5

mm in dia, mainly inv upper & posterior lung zones.

GGO20% calcify centrallyLymphadenopathy is commonEggshell calcification of hilar nodes (5%) DDx: Sarcoidosis

SILICOSIS

2 clinical forms: Acute silicosis (alveolar silicoproteinosis) classic silicosis (chr interstitial reticulonodular disease)

simple complicated

OBSTRUCTIVE LUNG DISEASE LUNG CANCER

Silicotuberculosis

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)

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

CHRONIC SIMPLE SILICOSIS

10--20 years of dust exposureRt upper lobes--posterior lung zones

nodules are in perilymphatic distributioncentered along the bronchovascular

bundles, centriacinar portion of the lobule, & in the subpleural lung, where the nodules form these pseudoplaques.

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)

Simple silicosispseudoplaques

diffuse nodular opacities with relative sparing of the basal lung zones

HRCT shows numerous small nodules

Complicated Silicosis (PROGRESSIVE MASSIVE FIBROSIS)

large opacities >1 cm in diametermid 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 yearsmay calcify + cavitate (ischemic necrosis/TB)

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.

OBSTRUCTIVE LUNG DISEASE AND LUNG CANCER

chronic bronchitis, & Emphysema.

Tobacco smoking may cause an additive effect.

Silicotuberculosissynergistic relationship between silicosis + tuberculosis

Coal miners are exposed to dusts that contain a mixture of coal, mica and silica in varying proportions.

COAL WORKER PNEUMOCONIOSIS

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

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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

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Differentiate PMF from lung cancerClinically and radiologically importantbilateral occurrence : DDx with tumors or

tuberculosis Unilateral masses occur : DDx is difficult

Chest PA Shape of mass Calcification Satellite Nodules Course of PMF

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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

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Differentiate from lung cancerSatellite 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

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Differentiate from lung cancer

# MR imaging : useful

★ lung cancer vs PMFHigh 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

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.

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

refers to pulmonary fibrosis secondary to asbestos exp.

Risk factors: Longer (approx. 20 years) exposure to the amphibole fiber type.

not associated with smokingTwo large groups: serpentines (Chrysotile)and

amphiboles(crocidolite).

Asbestosis

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 effect on respiratory bronchioles, alveoli, and pleura.

Asbestos-related diseases

Benign

Pleural diseases 1.plaques2.diffuse pleural thickening 3.effusion4.calcification

Parenchymal diseases 1.Asbestosis [parenchymal

fibrosis caused by asbestos inhalation]2.Rounded atelectasis 3.Benign fibrotic masses4.Transpulmonary bands

Malignancy 1.Malignant mesothelioma 2.Bronchogenic carcinoma

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.

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

pleural plaques right side∕ rounded atelectasis

diffuse pleural thickening

Diaphragmatic pleural plaques

visceral pleural plaque in the right major fissure & curvilinear bands of hyperattenuation in the posterior subpleural area.

calcified pleural plaques hallmark of asbestos exposure.

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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)

Pleural effusionearliest manifestation -within 10 years of

exposure, usually transient but requires close follow-up .

AsbestosisParenchymal 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.

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.

RETICULAR INFILTRATES

HONEYCOMB LUNG

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

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ASBESTOSIS VS IPF

FAVORS ASBESTOSISPleural plaquesSubpleural branching opacitiesSubpleural curvilinear linesParenchymal bandsHomogeneous subpleural opacities

o Pleural plaqueso Sub pleural curvilinear

lineso Parenchymal bands

Traction bronchectasis

Bronchiloectasishoneycombing

ASBESTOSIS IPF

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

Comet tail sign

PARENCHYMAL BAND “CROWS FEET”

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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 

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MesotheliomaMesothelioma 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.

MesotheliomaRare.majority have no plaques.

crocidolite is more neoplastic than chrysotile.

small, pleural effusionpoor Prognosis.

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 .

Mesothelioma indicated by the central pleural effusion

 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. 

 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. 

Occupational Lung CancersAsbestosArsenicBischloromethyl

etherCoke oven fumesInsoluble Hexavalent

chromium cmpds

Soluble nickelMustard gasRadon daughters

asbestosis lower lobes cancer is more likely-squamous cell or adenocarcinoma Bronchogenic carcinoma is almost always associated with cigarette smoking

SIDEROSIS

inert iron oxide/metallic iron depositsdiffuse 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 micronodulesbranching linear structuresextensive ground-glass attenuation without zonal

predominance

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.

XRAY chest -50% patients normal.

Abnormal findings -hilar adenopathy,increased interstitial markings.

HRCT:GGO,parenchymal nodules,septal lines.

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

CONCLUSIONSILICOSIS--multiple small rounded opacities in upper lobes5% Eggshell calcification of hilar nodes.

Asbestosis--Pleural without parenchymal disease.B/l Parietal pleural plaques in the mid lung –mc.50% Pleural calcification.

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