Pneumoconiosis

SilicosisCoal Workers’ PneumoconiosisAsbestos-Related Disease

Silicosis

SilicosisOccupational Exposure

Crystalline silica (quartz) from mining of

Coal, Graphite, Iron

Tin, Uranium, Gold

Silver, Copper

Sand blasters

Iron and steel foundry workers

Ceramic workers

Tunneling

SilicosisPathophysiology

Silica particles ingested by alveolarmacrophages

Breakdown of macrophage releasesenzymes which produce fibrogenicresponse

SilicosisNatural History

Requires 10-20 years exposure before x-ray appearance

Radiographs frequently overestimatedegree of symptoms early

Silicosis has a progressive naturedespite cessation of dust exposure

SilicosisX-ray-1

Multiple small rounded opacities

Usually in upper lobes

May have ground glass appearance

May occasionally calcify centrally (20%)

SilicosisX-ray-2

Lymph node enlargement common

Eggshell calcification of hilar nodes (5%)

DDx: Sarcoidosis

Large opacities are conglomerations ofsmall opacities

Complicated SilicosisProgressive Massive Fibrosis (PMF)

Massive fibrosis and conglomerate massformation in upper lobes with scarringand retraction of hila upwards

Progressive Massive Fibrosis (PMF) maycavitate from tuberculosis or ischemicnecrosis

Compensatory emphysema in lower lungfields

Caplan’s Syndrome

Consists of large necrobiotic nodulessuperimposed on silicosis

More common with CWP

SilicosisComplications

Predisposes to TB

Exhibits “limited” evidence forcarcinogenesis in humans

Coal Workers’

Pneumoconiosis

Coal Workers’

Pneumoconiosis

Coal Workers’ Pneumoconiosis(CWP)

Originally silica was erroneously thoughtto cause CWP

Actually due to inhalation of pure carbon

Still referred to as anthrasilicosis oranthracosis although most coal in USA isbituminous

No progression in absence of exposure

CWPNatural History

Rounded opacities of CWP, foundpredominantly in the upper lobes, do notprogress in absence of more coal dust

Coal Worker’s PneumoconiosisClassification

Classification is by the InternationalLabor Organization’s (ILO’s) 1980classification (p,q,r, etc.)

Direct correlation between amount ofcoal dust contained in lungs andprofusion category

Simple:small nodulesComplicated: larger nodules or masses

Coal Worker’s PneumoconiosisPathophysiology

Coal dust is deposited in alveolarmacrophages

Migrate to, and leave coal dust depositsaround, respiratory bronchioles

Fibrous reaction occurs

Coal Workers’ PneumoconiosisX-ray

Small, rounded opacities

Upper lobe distribution

Associated with chronic bronchitis andcor pulmonale

Coal Worker’s PneumoconiosisPMF

Most often, nodules have irregularborders with scar emphysema

Formed by fusion of groups of smallernodules

High ash content in the lungs

Nodules with regular borders andwithout scar emphysema

Arise from the enlargement of single nodule

High carbon content and little ash in lung

Complicated CWP

Large masses in

Upper lobes or

Superior segments of lower lobes

Unlike silicosis, large upper lobelesions of CWP are single (rather thanconglomerate) black masses with liquidcore, not fibrous tissue core

Masses may undergo cavitation eitherfrom TB or ischemia

Asbestos-RelatedDisease

Asbestos ExposureGeneral

Salts of salicic acid

90% of asbestos in USA is whiteasbestos (chrysotile)

Occurs in

Automotive workers-brake linings

Shipfitters

Construction workers

Asbestos-Related DiseaseTypes of Fibers

Chrysotile (white asbestos)–benign

Crocidolite (blue/black asbestos) inSouth Africa/Australia–malignant

Crocidolite-small fibers-associated withmost pleural disease

Asbestos-Related DiseasePathophysiology

Asbestos particles invoke a hemorrhagicresponse in lung

Fibers then coated with a ferritin-likematerial resulting in ferruginous bodies

Damage to respiratory bronchioles andalveoli

Asbestos-Related DiseaseTypes of

Asbestos-related Pleural Disease

Asbestosis

Asbestos-related Malignancies

Asbestos-Related Pleural Disease

Pleural plaques

Diffuse pleural thickening

Pleural calcification

Pleural Effusion

Asbestos-Related Pleural DiseaseIncidence of Pleural Disease

Almost all have some pleural involvement

Pleural plaque65%

Diffuse pleural thickening17%

Calcification50%

Effusion21%

Pleural involvement without parenchymaldisease is common

Asbestos-Related Pleural DiseasePleural Plaques-1

Affects submesothelial layer of parietalpleura

Bilateral, mid-lung zone

Between 7th and 10th ribs

Diaphragmatic pleura

Spares apices

Asbestos-Related Pleural DiseasePleural Plaques-2

Plaques don’t usually calcify

Plaques alone are not associated withmalignancy

Appear either in “profile” or “en face”

Asbestos-Related Pleural DiseaseDiffuse Pleural Thickening-1

Diffuse thickening of parietal pleura

Involves diaphragmatic pleura, extends uplateral chest wall

Commonly obliterates costophrenic angles

Spares apices of lungs

DDX from TB

Asbestos-Related Pleural DiseaseDiffuse Pleural Thickening-2

Frequently the sequela of benign pleuraleffusion

Associated with rounded atelectasis

Asbestos-Related Pleural DiseasePleural Calcification

Pleural calcification occurs in about 50%with asbestos-related disease

Especially diaphragmatic pleura

Dense calcifications paralleling diaphragm-Pathognomonic

DDx: Talc exposure, hemothorax, old TBempyema (unilateral)

Asbestos-Related Pleural DiseasePleural Effusion

Effusion alone may occur early in disease(first 20 years) in about 3% of cases

Exudative

May be associated with chest pain

Involves visceral pleura as well

Does not mean mesothelioma

May be associated with rounded atelectasis

AsbestosisGeneral

Reserved for parenchymal lung disease

Fibrosis begins around bronchi andprogresses outward

Asbestosis

Interstitial lung disease

Rounded atelectasis

AsbestosisLocation

More common in lower lungs

More common subpleural

AsbestosisX-ray

Opacities are small and irregularly shaped

Not rounded as in silicosis

Prominent septal lines around 2° lobules

Cardiac silhouette may become shaggy

Hilar lymph nodes rarely affected

DDx from silicosis

AsbestosisHRCT

Multiple subpleural dot-likenodularities=subpleural lines

Fibrous bands

Subpleural pulmonary arcades

Honeycombing

Thickened interlobular lines

Ground-glass appearance

Asbestos-Related DiseaseRounded Atelectasis

Form of peripheral lobar collapse

Associated with pleural disease

Resembles mass

Usually at lung base

“Comet tail” appearance back to hilum

Asbestos-Related Malignancies

Bronchogenic carcinoma

Mesothelioma

Benign

Malignant

Carcinoma of the larynx or stomach

Asbestos-Related DiseaseLung Cancer

Either squamous cell oradenocarcinoma

Bronchogenic ca is almost alwaysassociated with cigarette smoking

90x more common in smokers, 5x morecommon in non-smokers

Frequently at lung base

Associated with increased risk ofstomach cancer

AsbestosisMesotheliomas-1

Benign mesotheliomas not related toasbestos exposure

Asbestos exposure found in 80% ofmalignant mesotheliomas

But other x-ray changes ofasbestosis found in only 30% ofpatients with mesothelioma

AsbestosisMesotheliomas-2

No relation between mesothelioma andsmoking

Most often due to crocidolite particles

Most often present as unilateral pleuraleffusions

During course of disease, pleural effusiondevelops in almost all patients withmesothelioma

Asbestos-Related DiseaseHRCT Findings

Curvilinear subpleural lines

Thickened interstitial short lines

Subpleural dependent densities

Parenchymal bands

Honeycombing

Ground-glass opacification