OccupationalLung

diseases

DrDeepakAggarwal
Dept.OfPulmonaryMedicine
 Tobediscussed.

Pneumoconiosis
HypersensitivityPneumonitis
 PNEUMOCONIOSIS
Pneumoconioses arepulmonarydiseasescaused
bymineraldustinhalationinworkplace

Thespecifictypesofpneumoconioses are
namedbythesubstanceinhaled
(e.g.,silicosis,asbestosis,anthracosis)
 PNEUMOCONIOSIS
MineralDustInducedLungDisease
Simple coal workers' pneumoconiosis: Coal mining
Coal dust
macules and nodules
Complicated coal workers' pneumoconiosis:
PMF

Sandblasting,
Silica Silicosis
quarrying, mining,
stone cutting,
foundry work,
ceramics

Asbestosis pleural effusions, pleural plaques, or Mining, milling,

Asbestos and fabrication of
diffuse fibrosis; mesothelioma; carcinoma of the
ores and
lung and larynx
materials;
installation and
removal of
insulation
 Fibrogenicpneumoconioses
"truepneumoconioses"

asbestosis berylliosis

talcosis
silicosis
kaolinpneumoconiosis.
hardmetaldisease
coalworkers'
aluminumfibrosis, pneumoconiosis
Shaver'sdisease
 Nonfibrogenicpneumoconioses
benignpneumoconioses

Causes:

antimony iron
barium tin
boricacid titanium
manganese bismuth
 PNEUMOCONIOSIS
Pathogenesis
Thedevelopmentofapneumoconiosisdependson

(1)theamountofdustretainedinthelungandairways
(2)thesize,shape,andbuoyancyoftheparticles
(3)solubilityandphysiochemicalreactivity
(4)thepossibleadditionaleffectsofotherirritants(e.g.,
concomitanttobaccosmoking)
 PNEUMOCONIOSIS

Pathogenesis
(1)Theamountofdustretainedinthelungsis
determinedby

dustconcentrationinsurroundingair
durationofexposure
effectivenessofclearancemechanisms
 PNEUMOCONIOSIS
Pathogenesis

(2)thesize,shape,andbuoyancyoftheparticles

Themostdangerousparticlesrangefrom1to5m in
diameterbecausetheymayreachtheterminalsmall
airwaysandairsacsandsettleintheirlinings
 PNEUMOCONIOSIS

(3)Thesolubilityandcytotoxicityofparticlesmodifythe
natureofthepulmonaryresponse

Smallerparticlestendtocauseacutelunginjury
Largerparticlesresistdissolutionandsomaypersistwithin
thelungparenchymaforyears tendtoevokefibrosing
collagenouspneumoconioses
 PNEUMOCONIOSIS
Pathogenesis
Thepulmonaryalveolarmacrophage isakey
cellularelementintheinitiationandperpetuation
oflunginjuryandfibrosis
Themorereactiveparticles triggerthe
macrophagestoreleaseanumberofproductsthat
mediateaninflammatoryresponse andinitiate
fibroblastproliferation andcollagendeposition
 PNEUMOCONIOSIS
Pathogenesis
(4)thepossibleadditionaleffectsofother
irritants(e.g.,concomitanttobaccosmoking)
tobaccosmokingworsenstheeffectsofall
inhaledmineraldusts
 Coalworkerpneumoconiosis
CoalWorkersPneumoconiosisIsDueto
InhalationofCarbonParticles
Associatedwithcoalminingindustry
Carbon+silica(anthracosilicosis)
 Findings

Thespectrumoflungfindingsincoalworkersiswide,
varyingfrom
(1) Asymptomaticanthracosis
(2) SimpleCWPwithlittletonopulmonary
dysfunction
(3) ComplicatedCWP(progressivemassive
fibrosis)
 Anthracosis (urbandwellers)
morphology
Carbonparticles(anthrocotic pigment)in
alveolarandinterstitialmacrophages,in
connectivetissueandlymphatics andlung
hilus.
Generallyasymptomatic
 SimpleCWP
Coalmacules (1to2mmindiameter,consistsofperibronchiolar carbon
ladenmacrophagesanddilatedterminalbronchiole
largercoalnodules(containssmallamountsofadelicatenetworkof
collagen
locatedprimarilyadjacenttorespiratorybronchioles

Microscopy:
Carbonladenmacrophages&delicatecollagenfibres
adjacenttorespiratorybronchiolesinitially(wheredust
settles),laterinterstium &alveoli
Dilatationofrespiratorybronchiolesfocaldustemphysema

Radiographicfindingofbilateralsmallparenchymal nodules
CXRtypicallyshowsupperlungfieldnodules
 ComplicatedCWP
Gross
Multiple.,>2cm,vdarkscars
Microscopy:
Densecollagenandcarbonpigment.
Centralnecrosis(+/)
ProgressiondoesNOTcorrelatewithamountofcoaldust
depositioninlungs.
Cigarettesmokingincreasesrateofdeteriorationof
pulmonaryfunction.
 Caplans syndrome
1st describedincoalworkers,maybeseenin
otherpneumoconiosis
??Immunopathologic mechanism
Rheumatoidarthritis(RA)+Rheumatoid
nodules(Caplan nodules)inthelung
Rheumatoidarthritis+pneumoconioses
Caplans nodule=necrosissurroundedby
fibroblasts,monocytes andcollagen
s/sRA>lungsymptoms
 Clinicalcourse
Usuallyasymptomaticwithlittledecreaseoflung
function
ProgressiveDyspnoea,cough,expectoration
PMFpulmonarydysfunction(restrictive)
Pulmonaryhypertension,cor pulmonale
Progressiveeveniffurtherexposuretodustis
prevented
chronicbronchitisandemphysema
NoassociationwithTBorcarcinoma
 Management
Diagnosisbypresenceofclinicalfeatures
alongwithhistoryofexposuretocoaldustof
themagnitudethatissufficienttocausethe
disease
Imaging,PFT,sputumexamination
Treatment:nospecifictreatment,removal
fromfurtherexposureisimportant.
Treatunderlyingairwaydisease
 Silicosis
Silica is silicon dioxide, the oxide of silicon,
chemical formula SiO2.
SiO2 is the most abundant mineral on
earth
Silicosis (alsoknownasGrinder'sdisease and
Potter'srot)isaformofoccupationallung
disease causedbyinhalationofcrystalline
silicadust,andismarkedbyinflammation and
scarringinformsofnodularlesions inthe
upperlobesofthelungs
 Itisfoundinsand,manyrockssuchasgranite,
sandstone,flintandslate,andinsomecoal
andmetallicores.

Thecutting,breaking,crushing,drilling,
grinding,orabrasiveblastingofthese
materialsmayproducefinesilicadust.
 Silicosis Foundrywork

 Silicosis Stonecutting

 Silicosis Tunnelconstruction
WorstsingleincidenceofsilicosisinU.S.
HawksNestTunnel,GauleyBridge,W.Va.,19301931

 Silicosis Sandblasting
Compressed air at high pressure is used to blow fine sand or
other abrasive material through a hardened spray nozzle. The
abrasive particles quickly eat away whatever they are directed
at, leaving a clean, matte surface.
DiseasesAssociatedwithExposureto
SilicaDust
Silicosis
Chronicsilicosis
Acceleratedsilicosis
Acutesilicosis(silicoproteinosis)(finedust,
intenseexposure,highsilica)
Progressivemassivefibrosis

ChronicObstructivePulmonaryDisease
Emphysema
Chronicbronchitis
Mineraldustinducedsmallairwaydisease
DiseasesAssociatedwithExposureto
SilicaDust
LungCancer
Mycobacterial Infection
ImmuneRelatedDiseases
Progressivesystemicsclerosis
Rheumatoidarthritis
Chronicrenaldisease
Systemiclupuserythematosus
 Silicosis

The most prevalent occupational disease in the

world.
The induction period between initial silica exposure
and development of radiographically detectable nodular
silicosis is usually >10 years. Shorter induction periods
are associated with heavy exposures, and acute silicosis
may develop within 6 months to 2 years following
massive silica exposure
 ThreetypesofSilicosis
Simple chronic silicosis

Most common form

After long-term exposure (10-20 years) to low amounts
of silica dust.
Nodules of chronic inflammation and scarring form in
the lungs and chest lymph nodes.
Patients often asymptomatic, seen for other reasons.
subdivided into:
simple
complicatedsilicosis(PMF)
Accelerated silicosis (= PMF, progressive
massive fibrosis)

Occurs after exposure to larger amounts of silica

over a shorter period of time (5-10 years).
Inflammation, scarring, and symptoms progress
faster in accelerated silicosis
Patients have symptoms, especially shortness
of breath.
 Acute silicosis

From short-term exposure to very large

amounts of fine silica dust.
The lungs become very inflamed, causing
severe shortness of breath and low blood
oxygen level.
Killed hundreds of workers during Hawks
Nest Tunnel construction in early 1930s.
 CLINICALFEATURES
Themainsymptomisbreathlessness,firstnoted
duringexertionandlateratrestasthelarge
workingreserveofthelungisdiminished.
apatientwithchronicsilicosismaypresent
withoutsymptoms forassessmentofan
abnormalchestradiograph
Coughandsputumproduction arecommon
symptomsandusuallyrelatetochronicbronchitis
Clubbing isalsonotafeatureofsilicosis
 Patientswithsilicosisareparticularly
susceptibletotuberculosis (TB)infection
knownassilicotuberculosis.Thereasonfor
theincreasedrisk 1030foldincreased
incidence isnotwellunderstood.Itis
thoughtthatsilicadamagespulmonary
macrophages,inhibitingtheirabilitytokill
mycobacteria
 DiagnosisofSilicosis
Ingeneral,threekeyelementsplayarolein
thediagnosisofsilicosis:
Ahistoryofsilicaexposure sufficienttocause
thedegreeofillnessandtheappropriate
latencyfromthetimeoffirstexposure
Chestimaging(usuallyaconventionalchest
radiograph)thatshowsopacitiesconsistent
withsilicosis
Absenceofanotherdiagnosis morelikelyto
beresponsiblefortheobservedabnormalities
 Pulmonaryfunctiontestsarehelpfultogauge
severityofimpairment,butNOTfordiagnosis.
Lungbiopsyrarelyindicated(sincenoeffective
treatment,biopsyisdoneonlywhenother
diagnosesarebeingconsidered)
 Silicosiscanbemisdiagnosed
Silicosiscanmimic:
Sarcoidosis (benigninflammationofunknowncause)
Idiopathicpulmonaryfibrosis(lungscarringofunknown
cause)
Lungcancer
Severalotherlungconditions(chronicinfection,collagen
vasculardisease,etc.)

Can usually make right diagnosis with

detailed history (occupational & medical)
or, rarely, a lung biopsy.
 Thethreemainradiographicpresentations of
silicosisare:
simplesilicosis
progressivemassivefibrosis
silicoproteinosis
 Simplesilicosisreferstoaprofusionofsmall
(lessthan10mmindiameter)nodular
opacities(nodules).Thenodulesaregenerally
roundedbutcanbeirregular,andare
distributedpredominantlyintheupperlung
zones
Eggshellcalcification almost
exclusivelysilicosis
 Progressivemassivefibrosis(PMF,or
conglomeratesilicosis)occurswhenthese
smallopacitiesgraduallyenlargeandcoalesce
toformlarger,upper ormidzoneopacities
morethan10mmindiameter
Thehila areretractedupwardinassociation
withupperlobefibrosisandlowerlobe
hyperinflation
 Silicoproteinosis
Silicoproteinosisoccursfollowing
overwhelmingexposuretorespirable
crystallinesilicaoverashorttime,andisthe
radiographichallmarkofacutesilicosisThe
chestradiographdemonstratesa
characteristicbasilaralveolarfillingpattern,
withoutroundedopacitiesorlymphnode
calcifications.
 Treatment
Silicosisisanirreversibleconditionwithnocure.
Treatmentoptionscurrentlyfocusonalleviating
thesymptomsandpreventingcomplications
Thediseasewillgenerallyprogressevenwithout
furtherexposure,but therateofdeteriorationis
probablyreduced
Treatmentofallformsofsilicosisshouldbe
directedtowardcontrolofmycobacterial disease.
Lunglavage,transplantation
Preventionisthekey
 Asbestosis
Thepulmonaryparenchymalfibrosisdevelops
mostlyinthebases.
Generallyoccurswith>10years exposure,butthe
latencyperiodcanbe>30years.
Smokinghasasynergisticeffectwithasbestosisin
thedevelopmentoflungcancer.
ClinicallyisindistinguishablefromIPF
AssociatedlungCA:Squamousand
adenocarcinoma,NOTsmallorlargecell.
 Asbestosisafibroushydratedmagnesiumsilicate
withmorethan3000commercialusesduetoits
indestructiblenature,fireresistance,and
spinnability
fireprooftextiles,asinsulationforboilersand
pipes,usedinpaper,paints,cloth,tape,filters,
andwireinsulation.Morerecently,asbestoshas
beenusedincementpipesandinfriction
materials,includingbrakelinings,androofingand
floorproducts.
 Manifestations
PleuralPlaque:mostcommon
Theyarefocal,irregular,raisedwhitelesionsfoundon
theparietaland,rarely,thevisceralpleura
commonlytheyoccurinthelateralandposterior
midlung zones, wheretheymayfollowribcontoursand
thediaphragm.
Histologically:paucityofcells,extensivecollagenfibrils
arrangedinabasketweavepattern,andathin
coveringofmesothelial cells
Usuallybilateralandremainstableovermonths
Notreatment;observationwithperiodicCXR
Asbestosexposure
 Pleural plaque. The dome of the
diaphragm is covered
by a smooth, pearly white, nodular plaque

Asbestos-related pleural plaques

Large, discrete fibrocalcific plaques are seen
on the pleural surface of the diaphragm
 DiffusePleuralthickening
thickwhitepeelthatcanencasesignificantpulmonary
structures.
diffusepleuralthickeningorfibrosisisadiseaseofthe
visceralpleura
Developseitherduetoconfluenceofpleuralplaques,
duetoextensionofsubpleural fibrosisorduetofibrotic
resoluation ofbenignpleuraleffusion.
Assymptomatic ormaycauses/s
Nospecifictherapy
 Roundedatelactasis
Rarecomplication
Itiscausedby
scarringofthe
visceralandparietal
pleuraandthe
adjacentlung,with
thepleuralreaction
foldingoveronitself.
 Malignancies
Mesothelioma:Malignantmesotheliomas areassociated
(80%)withasbestosexposure,andlatencyperiodcanbe
aslongas40years.Unlikeinasbestosis,itisNOT
associatedwithsmokingandtendstoberapidlyfatal

Lungcancer:besidessmokingtobacco,asbestos
exposurehasbeenlinkedtoincraesed incidenceof lung
cancer.

Adenocarcinoma:mostcommonhistologicaltype
 Asbestosis
Interstitialpneumonitis andfibrosiscaused
byexposuretoasbestosfibers.
Macrophageaccumulationisaprominent
featureofthiscellularity.
Theprevalenceofparenchymal asbestosis
amongasbestosworkersincreasesasthe
lengthofemploymentincreases.
 CourseofAsbestosis
depositionofAsbestosfibersatairway
bifurcationsandinrespiratorybronchioles

Macrophagesaccumlate inandaroundthe
bronchiolesandalveolarductscausing
alveolarmacrophagealveolitis

Highfibre load Lowfibre load

Incompletephagocytosis and Mostfibres arecleared

secretionofproinflammatory leavinglungunscarred
cytokines

Residualfibrosisensues
 Dependingonthedurationandintensityof
exposure,thelatentperiodforthe
developmentofsymptomscanvaryfrom1
decadeto2 3decades
Dyspnoea,cough,rales (bilateral,lateto
paninspiratory)heardbestatposteriorlung
bases
Bilateraldiffusereticulonodularpatternon
CXR
 CTscanthorax
1. curvilinearsubpleural Lines
2. increasedintralobular
septa
3. dependentopacities,
4. parenchymal bandsand
interlobularcorestructures
5. honeycombing.
 Diagnosis
Presenceofsymptomsalongwithhistoryof
exposuretoasbestos
Duration,onset,type,intensityofexposure
CXR/CT
PFT
 Bronchoscopy
Bronchoscopy:biopsy/Balmayshowthepresenceofcoated
asbestosfibres whicharecalledasasbestosbodies
Thepresenceofmorethanonecoatedfiberhasbeencitedasa
necessarycriterionforthepathologicaldiagnosisofasbestosis
 Treatment
Noestablishedtreatmentavailableforthe
disease
Medicalsurveillanceisrecommendeddueto
riskoflungcancerandmesothelioma
OrganicDust(Byssinosis/Brownlungdisease)

Causedbyinhalationofcotton,flax,orhempdust.
Notimmunerelated,nosensitizationisneeded.
Earlystage:occasionalchesttightness
Latestage:regularchesttightnesstowardtheendof
the1stdayoftheworkweekMondaychest
tightnessandmayslowlyincreasetoincludemore
days.
Tt:Earlyonmayfocusonreversingobstructive
diseasewithantihistaminesandbronchodilators.
Removalofcausativeagent.
 HypersensitivityPneumonitis
Animmunemediated
granulomatous
inflammatoryreactionto
organicantigensin the
alveoliandintherespiratory
bronchioles
Alsocalled:extrinsicallergic
alveolitis
Dx andetiologyisoften
inthehistory HRCTinAcuteHP
Examples of EAA Etiology

Farmer's lung mouldy hay

Saw mill worker's lung mouldy wood dust
Bird fancier's lung proteins in bird droppings
Mushroom workers lung spores, moulds
Malt workers lung mouldy malt
Humidifier lung contaminated humidifier
water
Cheese washer's lung Penicillium casei
Suberosis cork dust mould

Diisocyanate lung polyurethane hardeners

Hard metal worker's lung hard metal dust, cobalt
 Symptoms
flulikeillness
cough
highfever,chills
dyspnea,chesttightness
malaise,myalgia
48hoursafterexposure

Chronicdisease:dyspneainstrain,sputum
production,fatigue,anorexia,weightloss
 Acute:HypersensitivityPneumonitis

mayhavefebrileillness,tachypnea,coughandchest
tightness38hoursafterexposure.
Transienthypoxemiaandleukocytosismayoccur.
Hypoxemiamaybesevereifpersonsinhalelarge
quantitiesofantigen.
CXRmayshowsmallnoduaropacitiesorpatchy
infiltrates.
Symptomstypicallypeak24hoursafteronsetand
resolvein13days.
 ChronicHypersensitivityPneumonitis

Canconsistofconstitutionalsymptomssuchaswt
loss,feverandfatigue.
Radiographicfindingsmorec/wwithtypical
interstitialfibrosis dyspnea,bilateralcrackles,cxr
withreticulonodular opacitiesandhoneycombing,
poorresponsetosteroids.

Ofnote:eosinophilia isNOTcharacteristicof
hypersensitivitypneumonitis.
 EAA, clinical findings

Status dyspnea, cyanosis,

crepitant rales
digital glubbing (chronic form)
Chest X-ray normal or small nodules/diffuse infiltrates/
ground glass appearance
chronic form: pulmonary fibrosis
HRCT normal or ground glass appearance
centrilobular micronodules
lung function restriction, diffusing capacity decreases,
hypoxemia, obstruction, hyperreactivity
lab. tests rise of sedimentation rate,
leukocytosis, neutrophilia
BAL marked lymphocytosis,
T helper / T supressor cells decreased
EAA: HRCT, acute disease
EAA: HRCT, chronic disease
 Diagnosis
Main criteria
1. Exposure to arganic dust (history, spesific IgG
antibodies, work place measurements).
2. Typical symptoms
3. Chest X-ray findings

Additional criteria
1. Decreased diffusion capacity
2. Hypoxia during rest or decreasing during excercise
3. Restriction in spirometric values
4. Lung biopsy with findings of allergic alveolitis
5. Provocation test (at work place) positive

All main criteria and two of the additional ones are

needed for diagnosis.
 Treatment
Treatment:Removethepatientfromthe
offendingantigen.
ShortcourseCorticosteroidsmaybeofhelp
inacutedisease.