Pneumoconiosis (silicosis)

Mohammad Tohidi M.D.
Professor of Internal Medicine
Department of Pulmonary Medicine
Ghaem Hospital MUMS Mashhad
IRAN

Case Scenario(1Case Scenario(1((
 57 year old retired non-smoker man57 year old retired non-smoker man
referred with the cc of dry cough forreferred with the cc of dry cough for
1year.In addition he has had mild ED but1year.In addition he has had mild ED but
no other complaint. Past Hx & systemno other complaint. Past Hx & system
review were negative.His VS,general PE &review were negative.His VS,general PE &
chest exam were normal.Chest X raychest exam were normal.Chest X ray
showed diffuse reticulonodular patternshowed diffuse reticulonodular pattern
There were no hilar enlargement &There were no hilar enlargement &
calcification.calcification.

Case Scenario(2Case Scenario(2((
 HRCT scan of the lung revealed smallHRCT scan of the lung revealed small
rounded opacities & thickening ofrounded opacities & thickening of
alveolar septaalveolar septa
no ground glass pattern,hilarno ground glass pattern,hilar
adenopathyadenopathy
& pleural effusion.He had >30 years& pleural effusion.He had >30 years
Hx of stone cutting & grinding.WithHx of stone cutting & grinding.With
this Hx & immaging studies, in thethis Hx & immaging studies, in the
absence of another causes,diagnosisabsence of another causes,diagnosis
of simple silicosis was apparent.of simple silicosis was apparent.

DEFINITIONDEFINITION
 Silicosis is a fibrotic lung diseaseSilicosis is a fibrotic lung disease
attributable to the inhalation ofattributable to the inhalation of
crystalline silica,crystalline silica, usually in theusually in the
form ofform of quartzquartz and, lessand, less
commonly, as cristobalite andcommonly, as cristobalite and
tridymitetridymite
 Amorphous silica is relativelyAmorphous silica is relatively
nontoxicnontoxic

IntroductionIntroduction
 SilicosisSilicosis (also known as(also known as Grinder'sGrinder's
diseasedisease andand Potter's rotPotter's rot) is a form) is a form
ofof occupational lung diseaseoccupational lung disease causedcaused
by inhalation of crystalline silicaby inhalation of crystalline silica
dust, and is marked bydust, and is marked by inflammationinflammation
andand scarring in forms of nodularscarring in forms of nodular
lesionslesions in the upper lobes of thein the upper lobes of the
lungslungs..

Where’s it come fromWhere’s it come from??
Crystalline forms of silicaCrystalline forms of silica (Silicon(Silicon
Dioxide or SiO2)Dioxide or SiO2) include quartz,include quartz,
cristobalite, and tridymite.cristobalite, and tridymite.
Quartz is the most common type,Quartz is the most common type,
and is a major component ofand is a major component of
rocks including granite, slate,rocks including granite, slate,
and sandstone.and sandstone.

SilicaSilica
 Silica is the second mostSilica is the second most
common mineral on earthcommon mineral on earth..
It is found in sand, manyIt is found in sand, many
rocks such as granite,rocks such as granite,
sandstone, flint and slate,sandstone, flint and slate,
and in some coal andand in some coal and
metallic ores.metallic ores.

SilicaSilica
 The cutting, breaking,The cutting, breaking,
crushing, drilling, grinding,crushing, drilling, grinding,
or abrasive blasting ofor abrasive blasting of
these materials maythese materials may
produce fine silica dust.produce fine silica dust.

Silicosis – historySilicosis – history
 This respiratory diseaseThis respiratory disease
was first recognized inwas first recognized in
1705 by1705 by RamazziniRamazzini whowho
noticed sand-likenoticed sand-like
substances in the lungssubstances in the lungs
of stonecuttersof stonecutters

Full description byFull description by
Bernardino RamazziniBernardino Ramazzini
(1633-1714) in early(1633-1714) in early
1818thth
century.century. ““...when...when
the bodies of suchthe bodies of such
workers areworkers are
dissected, they havedissected, they have
been found to bebeen found to be
stuffed with smallstuffed with small
stones.stones.”” Diseases ofDiseases of
Workers (De MorbisWorkers (De Morbis
Artificum Diatriba,Artificum Diatriba,
1713).1713).

 The name silicosisThe name silicosis
(from the Latin silex(from the Latin silex
or flint) wasor flint) was
attributed toattributed to ViscontiVisconti
in 1870in 1870

Silicosis - historySilicosis - history
 First U.S. description in 19First U.S. description in 19thth
century.century.
 Term silicosis introduced in 1870, from LatinTerm silicosis introduced in 1870, from Latin silexsilex, or flint., or flint.
 Prevalence increased markedly with introduction ofPrevalence increased markedly with introduction of
mechanized mining.mechanized mining.
 Came to national attention 1930-1931 with construction ofCame to national attention 1930-1931 with construction of
HawkHawk’’s Nest Tunnel in Gauley Bridge, West Virginia. Calleds Nest Tunnel in Gauley Bridge, West Virginia. Called
““the worst industrial accident in U.S. history.the worst industrial accident in U.S. history.”” At least 764At least 764
tunnel workers died from silicosis. Hawktunnel workers died from silicosis. Hawk’’s Nest disaster led tos Nest disaster led to
Congressional hearings in 1936, and new laws protectingCongressional hearings in 1936, and new laws protecting
workers in many states.workers in many states.
 Prevalence of silicosis has greatly declined in recent decadesPrevalence of silicosis has greatly declined in recent decades
because of effective industrial hygiene measures.because of effective industrial hygiene measures.

 The full name for this diseaseThe full name for this disease
when caused by the specificwhen caused by the specific
exposure to fine silica dustexposure to fine silica dust
found in volcanoes isfound in volcanoes is
pneumonoultramicroscopicsilicovpneumonoultramicroscopicsilicov
, and at 45 letters it is the, and at 45 letters it is the
longest word in any of thelongest word in any of the
major English dictionaries.major English dictionaries.

 The prevalence of silicosisThe prevalence of silicosis
led some men to growled some men to grow
what is called awhat is called a miner'sminer's
mustachemustache, in an attempt to, in an attempt to
intercept as much dust asintercept as much dust as
possible.possible.

Diseases Associated withDiseases Associated with
Exposure to Silica Dust(1Exposure to Silica Dust(1((
 SilicosisSilicosis
Chronic silicosisChronic silicosis
Accelerated silicosisAccelerated silicosis
Acute silicosis (silicoproteinosis)(fine dust,Acute silicosis (silicoproteinosis)(fine dust,
intense exposure , high silica)intense exposure , high silica)
Progressive massive fibrosisProgressive massive fibrosis
 Chronic Obstructive Pulmonary DiseaseChronic Obstructive Pulmonary Disease
EmphysemaEmphysema
Chronic bronchitisChronic bronchitis
Mineral dust-induced small airway diseaseMineral dust-induced small airway disease

Diseases Associated withDiseases Associated with
Exposure to Silica Dust(2Exposure to Silica Dust(2((
Lung CancerLung Cancer
Mycobacterial InfectionMycobacterial Infection
Mycobacterium tuberculosisMycobacterium tuberculosis
NontuberculousNontuberculous MycobacteriaMycobacteria
Immune-Related DiseasesImmune-Related Diseases
Progressive systemic sclerosisProgressive systemic sclerosis
Rheumatoid arthritisRheumatoid arthritis
Chronic renal diseaseChronic renal disease
Systemic lupus erythematosusSystemic lupus erythematosus

Pulmonary ToxicologyPulmonary Toxicology
•• Particle size is critical.Particle size is critical.
•• Peak dust inhalationPeak dust inhalation
occurs with particlesoccurs with particles
having a diameter of 0.5 tohaving a diameter of 0.5 to
3 microns (μm).3 microns (μm).
•• RCS is invisible to theRCS is invisible to the
human eye.human eye.
•• Pulmonary clearancePulmonary clearance
mechanisms:mechanisms:
macrophages & themacrophages & the
mucociliary escalatormucociliary escalator

 The induction period between initialThe induction period between initial
silica exposure and development ofsilica exposure and development of
radiographically detectable nodularradiographically detectable nodular
silicosis is usuallysilicosis is usually 10 years10 years. Shorter. Shorter
induction periods are associated withinduction periods are associated with
heavy exposures, and acute silicosisheavy exposures, and acute silicosis
may develop withinmay develop within 6 months to 26 months to 2
years following massive silicayears following massive silica
exposureexposure..

 Silicosis is an occupationalSilicosis is an occupational
hazard to mining,hazard to mining,
sandblasting, quarry,sandblasting, quarry,
ceramics and foundryceramics and foundry
workers, as well as grinders,workers, as well as grinders,
stonecutters and thosestonecutters and those
continually exposed to silicacontinually exposed to silica
dust.dust.

Variety of occupationsVariety of occupations
 Construction, and surface andConstruction, and surface and
underground rock drillingunderground rock drilling
 Foundries are also a main source ofFoundries are also a main source of
silica dustsilica dust
 workers involved with the repair,workers involved with the repair,
rehabilitation, or demolition ofrehabilitation, or demolition of
concrete structuresconcrete structures

Variety of occupationsVariety of occupations
 New types of pneumoconiosis oftenNew types of pneumoconiosis often
turn out to be silicosis in an industryturn out to be silicosis in an industry
not previously thought to be at risknot previously thought to be at risk
or aor a mixed-dust pneumoconiosismixed-dust pneumoconiosis inin
which silica is implicated with otherwhich silica is implicated with other
dustsdusts
 Silicosis is often the result ofSilicosis is often the result of
exposure inexposure in the remote pastthe remote past and notand not
in the current workplacein the current workplace

Pathology(1Pathology(1((
 When small silica dust particlesWhen small silica dust particles
are inhaled, they can embedare inhaled, they can embed
themselves deeply into the tinythemselves deeply into the tiny
alveolar sacs and ducts in thealveolar sacs and ducts in the
lungs, where oxygen and carbonlungs, where oxygen and carbon
dioxide gases are exchanged.dioxide gases are exchanged.
There, the lungs cannot clear outThere, the lungs cannot clear out
the dust by mucous or coughingthe dust by mucous or coughing

 Characteristic lung tissueCharacteristic lung tissue
pathology in nodular silicosispathology in nodular silicosis
consists of fibrotic nodules withconsists of fibrotic nodules with
concentric "onion-skinned"concentric "onion-skinned"
arrangement ofarrangement of collagencollagen fibers,fibers,
central hyalinization, and acentral hyalinization, and a
cellular peripheral zone,cellular peripheral zone, withwith
lightlylightly birefringent particlesbirefringent particles seenseen
under polarized lightunder polarized light

 In acute silicosis, microscopicIn acute silicosis, microscopic
pathology shows a periodicpathology shows a periodic
acid-Schiff positive alveolaracid-Schiff positive alveolar
exudate (alveolarexudate (alveolar
lipoproteinosis) and a cellularlipoproteinosis) and a cellular
infiltrate of the alveolar wallsinfiltrate of the alveolar walls

PATHOGENESIS(1PATHOGENESIS(1((
1.1. There is agreement thatThere is agreement that freshly fracturedfreshly fractured
silica,silica, such as that generated duringsuch as that generated during
sandblastingsandblasting, is more toxic to the, is more toxic to the
alveolar macrophages than isalveolar macrophages than is "aged""aged"
silicasilica
2.2. clay componentsclay components, may adhere to the, may adhere to the
surfaces of silica particles, producingsurfaces of silica particles, producing
"coated" silica"coated" silica, which is less toxic than, which is less toxic than
uncoated silica dustuncoated silica dust
3.3. the incidence of silicosis is decreased bythe incidence of silicosis is decreased by
concomitant exposure to other dustsconcomitant exposure to other dusts

PATHOGENESIS(2PATHOGENESIS(2((
4 The4 The intensity of the exposureintensity of the exposure
determines the nature of the lungdetermines the nature of the lung
injury. Low-intensity exposureinjury. Low-intensity exposure
generally produces aggregates ofgenerally produces aggregates of
fibrosis with relative sparing of thefibrosis with relative sparing of the
lung architecture, whereaslung architecture, whereas high-high-
intensity exposure causesintensity exposure causes
widespread pulmonarywidespread pulmonary
inflammation and collageninflammation and collagen
depositiondeposition
5 Individual susceptibility to the5 Individual susceptibility to the
diseasedisease may play a rolemay play a role

Particles engulfed byParticles engulfed by
macrophages:macrophages:
transported upward and removed from lungstransported upward and removed from lungs
retained in the lungretained in the lung ““FrustratedFrustrated
PhagocytosisPhagocytosis””
cascade of toxic effectscascade of toxic effects
inflammatory processinflammatory process
pneumoconiosispneumoconiosis

Pathogenesis(3Pathogenesis(3((
 When fine particles of silica dust areWhen fine particles of silica dust are
deposited in the lungs,deposited in the lungs, macrophagesmacrophages thatthat
ingest the dust particles will set off aningest the dust particles will set off an
inflammationinflammation response by releasingresponse by releasing tumortumor
necrosis factorsnecrosis factors,, interleukin-1interleukin-1,,
leukotriene B4leukotriene B4 and otherand other cytokinescytokines. In. In
turn, these stimulateturn, these stimulate fibroblastsfibroblasts toto
proliferate and produce collagen aroundproliferate and produce collagen around
the silica particle, thus resulting inthe silica particle, thus resulting in fibrosisfibrosis
and the formation of the nodular lesionsand the formation of the nodular lesions

Pathogenesis(4Pathogenesis(4((
 Furthermore, the surface ofFurthermore, the surface of
silicon dust can generatesilicon dust can generate
silicon-based radicals thatsilicon-based radicals that
lead to the production oflead to the production of
hydroxylhydroxyl and oxygen radicals,and oxygen radicals,
as well asas well as hydrogen peroxidehydrogen peroxide,,
which can inflict damage towhich can inflict damage to
the surrounding cellsthe surrounding cells

 MC chronic occupational disease in the worldMC chronic occupational disease in the world
 caused bycaused by inhalation of crystalline silicon dioxide (silica).inhalation of crystalline silicon dioxide (silica).
 Acute silicosisAcute silicosis --accumulation of a lipoproteinaceous material within alveoliaccumulation of a lipoproteinaceous material within alveoli
 Chronic silicosisChronic silicosis - slowly progressing, nodular, Fibrosing pneumoconiosis- slowly progressing, nodular, Fibrosing pneumoconiosis
 PathogenesisPathogenesis
 crystalline forms -more fibrogenic (crystalline forms -more fibrogenic (quartzquartz ––worstworst))
 silica particlessilica particles lung macrophages ingest themlung macrophages ingest them  activation and release of mediatorsactivation and release of mediators  IL-1, TNF,IL-1, TNF,
oxygen-derived free radicalsoxygen-derived free radicals
 Anti-TNF monoclonal antibodies can block lung collagen accumulation in miceAnti-TNF monoclonal antibodies can block lung collagen accumulation in mice
 Morphology.Morphology.
• EarlyEarly stagesstages ––tiny nodules in the upper zonestiny nodules in the upper zones
• diseasedisease progressesprogresses ––nodules coalesce intonodules coalesce into hard, collagenous scarshard, collagenous scars central softening andcentral softening and
cavitation (due to superimposed tuberculosis or to ischemia)cavitation (due to superimposed tuberculosis or to ischemia)
• X-rayX-ray –– egg shellegg shell calcification in the lymph nodescalcification in the lymph nodes
• Advanced stageAdvanced stage - PMF- PMF
 HistologyHistology
 Nodular lesions -concentric layers of hyalinized collagen surrounded by a dense capsuleNodular lesions -concentric layers of hyalinized collagen surrounded by a dense capsule
 Birefringent silica particles in polarized microscopyBirefringent silica particles in polarized microscopy

EPIDEMIOLOGYEPIDEMIOLOGY
 The prevalence of silicosis is difficult toThe prevalence of silicosis is difficult to
estimateestimate
 the reported cases have been estimated tothe reported cases have been estimated to
represent onlyrepresent only one thirdone third of the total casesof the total cases
of silicosisof silicosis
 In calculating an individual's risk forIn calculating an individual's risk for
silicosis,silicosis, durationduration andand intensity ofintensity of
exposureexposure are of primary interest butare of primary interest but peakpeak
exposureexposure also may be important.also may be important.

EPIDEMIOLOGY(cont’dEPIDEMIOLOGY(cont’d((
 In the United States, NIOSH hasIn the United States, NIOSH has
estimated that at leastestimated that at least 1.7 million1.7 million
workersworkers are exposed to silica, ofare exposed to silica, of
whom between 1500 and 2360 willwhom between 1500 and 2360 will
develop silicosis each yeardevelop silicosis each year

PrevalencePrevalence
 Silicosis is theSilicosis is the mostmost
common occupational lungcommon occupational lung
disease worldwide,disease worldwide, itit
occurs everywhere but isoccurs everywhere but is
especially common inespecially common in
developing countriesdeveloping countries

Silicosis deaths - decliningSilicosis deaths - declining
www.cdc.gov/mmwrwww.cdc.gov/mmwr
1,157 (1968( 148 (20021,157 (1968( 148 (2002((

CLINICAL FEATURES(1CLINICAL FEATURES(1((
 The main symptom isThe main symptom is breathlessnessbreathlessness, first, first
noted during exertion and later at rest asnoted during exertion and later at rest as
the large working reserve of the lung isthe large working reserve of the lung is
diminished. In chronic silicosis, in thediminished. In chronic silicosis, in the
absence of other respiratory disease, evenabsence of other respiratory disease, even
this symptom may be absentthis symptom may be absent
 a patient with chronic silicosis may presenta patient with chronic silicosis may present
without symptomswithout symptoms for assessment of anfor assessment of an
abnormal chest radiographabnormal chest radiograph

 The appearance of breathlessness mayThe appearance of breathlessness may
mark the development of a complicationmark the development of a complication
such as progressive massive fibrosis orsuch as progressive massive fibrosis or
tuberculosis, or may reflect associatedtuberculosis, or may reflect associated
airway diseaseairway disease
 Cough and sputum productionCough and sputum production areare
common symptoms and usuallycommon symptoms and usually
relate to chronic bronchitis, but mayrelate to chronic bronchitis, but may
reflect the development ofreflect the development of
tuberculosis or lung cancertuberculosis or lung cancer

 Chest painChest pain is not a feature ofis not a feature of
silicosis, nor are systemic symptomssilicosis, nor are systemic symptoms
such assuch as fever and weight lossfever and weight loss, which, which
should be attributed to tuberculosisshould be attributed to tuberculosis
or lung cancer until provenor lung cancer until proven
otherwise.otherwise.
 ClubbingClubbing is also not a feature ofis also not a feature of
silicosissilicosis

 In accelerated and acute silicosis,In accelerated and acute silicosis, the timethe time
scale of symptom evolutionscale of symptom evolution isis in years orin years or
months rather than decadesmonths rather than decades. In acute. In acute
silicosis, breathlessness may becomesilicosis, breathlessness may become
disabling within months, followed bydisabling within months, followed by
impaired gas exchangeimpaired gas exchange CyanosisCyanosis
Cor pulmonaleCor pulmonale
Respiratory insufficiencyRespiratory insufficiency

 Patients with silicosis are particularlyPatients with silicosis are particularly
susceptible to tuberculosis (TB)susceptible to tuberculosis (TB)
infection - known asinfection - known as
silicotuberculosis. The reason for thesilicotuberculosis. The reason for the
increased risk -increased risk - 10-30 fold increased10-30 fold increased
incidenceincidence - is not well understood. It- is not well understood. It
is thought thatis thought that silica damagessilica damages
pulmonary macrophages, inhibitingpulmonary macrophages, inhibiting
their ability to kill mycobacteriatheir ability to kill mycobacteria

Types of SilicosisTypes of Silicosis
(1) Chronic silicosis(1) Chronic silicosis
Occurs after 15-20 years of exposureOccurs after 15-20 years of exposure
to moderate to low levels of silicato moderate to low levels of silica
dust. Chronic silicosis itself is furtherdust. Chronic silicosis itself is further
subdivided into:subdivided into:
simplesimple
complicated silicosis(PMF)complicated silicosis(PMF)

Chronic silicosisChronic silicosis
 This is the most commonThis is the most common
type of silicosis. Patients withtype of silicosis. Patients with
this type of silicosis may notthis type of silicosis may not
have obvious symptoms, so ahave obvious symptoms, so a
chest X-ray is necessarychest X-ray is necessary toto
determine if there is lungdetermine if there is lung
damage.damage.

(2) Asymptomatic silicosis(2) Asymptomatic silicosis
Early cases of the disease doEarly cases of the disease do
not present any symptomsnot present any symptoms

(3) Accelerated silicosis(3) Accelerated silicosis
Silicosis that develops 5-10Silicosis that develops 5-10
years after high exposure toyears after high exposure to
silica dust. Symptoms includesilica dust. Symptoms include
severe shortness of breath,severe shortness of breath,
weakness, and weight lossweakness, and weight loss

(4) Acute silicosis(4) Acute silicosis
Silicosis that developsSilicosis that develops
a few months to 2 yearsa few months to 2 years
after exposure to very highafter exposure to very high
concentrations of silicaconcentrations of silica
dust.dust.

Diagnosis of SilicosisDiagnosis of Silicosis
 In general, three key elements play a roleIn general, three key elements play a role
in the diagnosis of silicosis:in the diagnosis of silicosis:
 A history of silica exposureA history of silica exposure sufficient tosufficient to
cause the degree of illness and thecause the degree of illness and the
appropriate latency from the time of firstappropriate latency from the time of first
exposureexposure
 Chest imaging (usually a conventionalChest imaging (usually a conventional
chest radiograph) that showschest radiograph) that shows opacitiesopacities
consistent with silicosisconsistent with silicosis
 Absence of another diagnosisAbsence of another diagnosis more likelymore likely
to be responsible for the observedto be responsible for the observed
abnormalitiesabnormalities

Diagnosis of SilicosisDiagnosis of Silicosis
 Abnormal chest X-ray (or chest CT scan)Abnormal chest X-ray (or chest CT scan)
consistent with silicosisconsistent with silicosis
 History ofHistory of significantsignificant exposure to silica dustexposure to silica dust
 Medical evaluation to exclude other possibleMedical evaluation to exclude other possible
causes of abnormal chest x-raycauses of abnormal chest x-ray
 Pulmonary function tests are helpful toPulmonary function tests are helpful to
gauge severity of impairment, but NOT forgauge severity of impairment, but NOT for
diagnosis.diagnosis.
 Lung biopsy rarely indicatedLung biopsy rarely indicated (since no(since no
effective treatment, biopsy is done onlyeffective treatment, biopsy is done only
when other diagnoses are being considered)when other diagnoses are being considered)

Silicosis can be misdiagnosedSilicosis can be misdiagnosed
 Silicosis can mimic:Silicosis can mimic:
• Sarcoidosis (benign inflammation of unknownSarcoidosis (benign inflammation of unknown
cause)cause)
• Idiopathic pulmonary fibrosis (lung scarring ofIdiopathic pulmonary fibrosis (lung scarring of
unknown cause)unknown cause)
• Lung cancerLung cancer
• Several other lung conditions (chronicSeveral other lung conditions (chronic
infection, collagen-vascular disease, etc.)infection, collagen-vascular disease, etc.)
Can usually make right diagnosis withCan usually make right diagnosis with
detailed history (occupational & medical)detailed history (occupational & medical)
or, rarely, a lung biopsy.or, rarely, a lung biopsy.

LUNG FUNCTIONLUNG FUNCTION
 The lung function profile isThe lung function profile is
determined by the extent of silicosisdetermined by the extent of silicosis
as well as associated or concomitantas well as associated or concomitant
airway and vascular changesairway and vascular changes
 In chronic silicosis, spirometric testsIn chronic silicosis, spirometric tests
(FEV1, FEV1/FVC, and maximal(FEV1, FEV1/FVC, and maximal
midexpiratory flow) usually reflectmidexpiratory flow) usually reflect
airflow limitation.airflow limitation.

 In the accelerated and acute forms,In the accelerated and acute forms,
functional changes are more markedfunctional changes are more marked
and progression is more rapid.and progression is more rapid. InIn
acute silicosis, lung function shows aacute silicosis, lung function shows a
restrictive defect and impairment ofrestrictive defect and impairment of
gas exchange, which leads togas exchange, which leads to
respiratory failurerespiratory failure and eventually toand eventually to
death from intractable hypoxemiadeath from intractable hypoxemia

 Reduction in diffusing capacityReduction in diffusing capacity isis
generally apparent in more advancedgenerally apparent in more advanced
chronic silicosis and probably reflectschronic silicosis and probably reflects
associated emphysema.associated emphysema.
 It is possible that most of the lungIt is possible that most of the lung
function changes associated withfunction changes associated with
chronic silicosis can be attributed tochronic silicosis can be attributed to
thethe associated emphysema.associated emphysema.

Chest imagingChest imaging
 TheThe three main radiographicthree main radiographic
presentationspresentations of silicosis are:of silicosis are:
simple silicosissimple silicosis
progressive massive fibrosisprogressive massive fibrosis
silicoproteinosissilicoproteinosis

Simple silicosisSimple silicosis
 Simple silicosis refers to a profusionSimple silicosis refers to a profusion
of small (less than 10 mm inof small (less than 10 mm in
diameter) nodular opacitiesdiameter) nodular opacities
(nodules). The nodules are generally(nodules). The nodules are generally
rounded but can be irregular, androunded but can be irregular, and
are distributed predominantly in theare distributed predominantly in the
upper lung zonesupper lung zones

Progressive massive fibrosisProgressive massive fibrosis
 Progressive massive fibrosis (PMF, orProgressive massive fibrosis (PMF, or
conglomerate silicosis) occurs whenconglomerate silicosis) occurs when
these small opacities graduallythese small opacities gradually
enlarge and coalesce to form larger,enlarge and coalesce to form larger,
upper- or mid-zone opacities moreupper- or mid-zone opacities more
than 10 mm in diameterthan 10 mm in diameter

PMFPMF
 The hila are retracted upward inThe hila are retracted upward in
association with upper lobe fibrosis andassociation with upper lobe fibrosis and
lower lobe hyperinflationlower lobe hyperinflation
 Hilar adenopathy with prominentHilar adenopathy with prominent
calcification is often present. The opacitiescalcification is often present. The opacities
of PMF can beof PMF can be asymmetricalasymmetrical, and may, and may
mimic a neoplastic process.mimic a neoplastic process. CavitationCavitation
may also be present in advanced disease,may also be present in advanced disease,
or in the setting of mycobacterialor in the setting of mycobacterial
superinfectionsuperinfection

SilicoproteinosisSilicoproteinosis
 Silicoproteinosis occurs followingSilicoproteinosis occurs following
overwhelming exposure to respirableoverwhelming exposure to respirable
crystalline silica over a short time,crystalline silica over a short time,
and is the radiographic hallmark ofand is the radiographic hallmark of
acute silicosis The chest radiographacute silicosis The chest radiograph
demonstrates a characteristic basilardemonstrates a characteristic basilar
alveolar filling pattern, withoutalveolar filling pattern, without
rounded opacities or lymph noderounded opacities or lymph node
calcifications.calcifications.

HRCTHRCT
 There is general agreementThere is general agreement
that CT/HRCT is superior tothat CT/HRCT is superior to
conventional chestconventional chest
radiography forradiography for
documentation of PMF lesionsdocumentation of PMF lesions
and emphysematous changesand emphysematous changes
associated with silicosisassociated with silicosis

 pleural effusions are unusual,butpleural effusions are unusual,but
pleural thickening appears to bepleural thickening appears to be
common, especially among patientscommon, especially among patients
with more severe disease. In a serieswith more severe disease. In a series
of 110 patients with biopsy provenof 110 patients with biopsy proven
silicosis followed for a mean of 14silicosis followed for a mean of 14
years,years, pleural effusions were notedpleural effusions were noted
in 12 patients (11 percent),in 12 patients (11 percent), butbut
pleural thickening was present in 64pleural thickening was present in 64
patients (58 percent)patients (58 percent)

Normal SimpleNormal Simple
silicosissilicosis
n

Accelerated SilicosisAccelerated Silicosis
( Progressive Massive Fibrosis)( Progressive Massive Fibrosis)
normal chest x-raynormal chest x-ray PMFPMF

Accelerated Silicosis (PMF)Accelerated Silicosis (PMF)
chest x-ray CT scanchest x-ray CT scan


Eggshell calcification – almostEggshell calcification – almost
exclusively silicosisexclusively silicosis

RADIOGRAPHIC FEATURES(2RADIOGRAPHIC FEATURES(2((
 Silicotic nodules are usually,Silicotic nodules are usually,
although not invariably,although not invariably,
symmetrically distributedsymmetrically distributed and tend toand tend to
occur first in theoccur first in the upper zonesupper zones .later,.later,
although not invariably, other zonesalthough not invariably, other zones
are involved. Occasionally theare involved. Occasionally the
nodules arenodules are calcifiedcalcified, resembling, resembling
microlithiasismicrolithiasis

 Enlargement of the hilar nodesEnlargement of the hilar nodes maymay
precede the development of theprecede the development of the
parenchymal lesionsparenchymal lesions. ". "Eggshell"Eggshell"
calcificationcalcification, when present, is, when present, is
strongly suggestive although notstrongly suggestive although not
pathognomonic, of silicosispathognomonic, of silicosis
 Pleural plaquesPleural plaques may occur but aremay occur but are
not a common feature.not a common feature.

 Progressive massive fibrosis isProgressive massive fibrosis is
characterized by thecharacterized by the coalescence ofcoalescence of
small rounded opacities to formsmall rounded opacities to form
larger lesionslarger lesions they are graded on thethey are graded on the
ILO scale according to size andILO scale according to size and
extent (categories A to C).extent (categories A to C).

 CT assessment is superior to the chestCT assessment is superior to the chest
radiograph not only in assessing theradiograph not only in assessing the
presence andpresence and extent of silicotic nodulationextent of silicotic nodulation,,
but also in revealingbut also in revealing early conglomerationearly conglomeration..
 With time, the mass lesions tend toWith time, the mass lesions tend to
contract, usually to the upper lobes,contract, usually to the upper lobes,
leavingleaving hypertranslucent zoneshypertranslucent zones at theirat their
margins and often at the lung bases. Inmargins and often at the lung bases. In
this process, small rounded opacities,this process, small rounded opacities,
previously evident, maypreviously evident, may disappeardisappear,,
resulting in a picture that needs to beresulting in a picture that needs to be
distinguished from tuberculosisdistinguished from tuberculosis

 The rapid development ofThe rapid development of severalseveral
large lesionslarge lesions suggestssuggests rheumatoidrheumatoid
silicosissilicosis, but new lesions, especially if, but new lesions, especially if
cavitated, should be regarded ascavitated, should be regarded as
evidence of mycobacterial diseaseevidence of mycobacterial disease
 Acute silicosis is characterizedAcute silicosis is characterized
radiologically by diffuse changes thatradiologically by diffuse changes that
usually display anusually display an air space andair space and
interstitial patterninterstitial pattern rather than therather than the
usual nodularityusual nodularity

Diagnosis: SerologyDiagnosis: Serology
 HypergammaglobulinemiaHypergammaglobulinemia
 RFRF
 ANFANF
 S-ACES-ACE
 Increased incidence of systemicIncreased incidence of systemic
sclerosissclerosis
described in SA gold minersdescribed in SA gold miners

TreatmentTreatment
 Silicosis is an irreversibleSilicosis is an irreversible
condition with no cure.condition with no cure.
Treatment options currentlyTreatment options currently
focus on alleviating thefocus on alleviating the
symptoms and preventingsymptoms and preventing
complicationscomplications

TreatmentTreatment
 The disease will generallyThe disease will generally
progress even withoutprogress even without
further exposure,but thefurther exposure,but the
rate of deterioration israte of deterioration is
probably reducedprobably reduced

TreatmentTreatment
 There is currently interest inThere is currently interest in
the use ofthe use of lung lavagelung lavage toto
remove silica from the lung,remove silica from the lung,
but a favorable impact onbut a favorable impact on
progression of acute orprogression of acute or
chronic silicosis has not beenchronic silicosis has not been
demonstrateddemonstrated..

TreatmentTreatment
 Treatment of all forms of silicosis shouldTreatment of all forms of silicosis should
be directed towardbe directed toward control ofcontrol of
mycobacterial disease.mycobacterial disease. This is especiallyThis is especially
true for acute and accelerated silicosis andtrue for acute and accelerated silicosis and
silicosis in workers with humansilicosis in workers with human
immunodeficiency virus infectionimmunodeficiency virus infection
 All patients with silicosis should have aAll patients with silicosis should have a
tuberculin skin test and, if it is positive, betuberculin skin test and, if it is positive, be
offered treatment for latent tuberculosisoffered treatment for latent tuberculosis
infectioninfection

TreatmentTreatment
 Interventions to interrupt theInterventions to interrupt the
inflammatory process that leads toinflammatory process that leads to
chronic silicosis including thechronic silicosis including the
inhalation of aluminuminhalation of aluminum oror
polyvinylpyridine-polyvinylpyridine-NN-oxide-oxide andand oraloral
tetrandinetetrandine havehave not been shown tonot been shown to
be successfulbe successful

TreatmentTreatment
 The interaction between silicaThe interaction between silica
exposure and smoking in theexposure and smoking in the
development of COPD makes itdevelopment of COPD makes it
particularly important to implementparticularly important to implement
smoking cessation programs in thesmoking cessation programs in the
workplaceworkplace

TreatmentTreatment
 Because acute and acceleratedBecause acute and accelerated
silicosis carry such a poor prognosissilicosis carry such a poor prognosis
and tend to occur in youngerand tend to occur in younger
persons, consideration should bepersons, consideration should be
given togiven to lung transplantationlung transplantation in suchin such
casescases

PreventionPrevention
 The best way to preventThe best way to prevent
silicosis is tosilicosis is to identify work-identify work-
place activitiesplace activities that producethat produce
crystalline silica dust andcrystalline silica dust and
thenthen to eliminate or controlto eliminate or control
the dust.the dust. Water sprayWater spray is oftenis often
used where dust emanates.used where dust emanates.
Dust can also be controlledDust can also be controlled
throughthrough dry air filteringdry air filtering

PreventionPrevention The most important aspect of theThe most important aspect of the
management of silicosis relates to itsmanagement of silicosis relates to its
preventionprevention
 a sustained effort must be made toa sustained effort must be made to
increase awareness of silicosisincrease awareness of silicosis..
Recent deaths from silicosis inRecent deaths from silicosis in
younger individuals in the Unitedyounger individuals in the United
States have occurred after exposureStates have occurred after exposure
in thein the construction andconstruction and
manufacturing sectorsmanufacturing sectors, with none, with none
from miningfrom mining

 MC chronic occupational disease in the worldMC chronic occupational disease in the world
 caused bycaused by inhalation of crystalline silicon dioxide (silica).inhalation of crystalline silicon dioxide (silica).
 Acute silicosisAcute silicosis --accumulation of a lipoproteinaceous material withinaccumulation of a lipoproteinaceous material within
alveolialveoli
 Chronic silicosisChronic silicosis - slowly progressing, nodular, Fibrosing pneumoconiosis- slowly progressing, nodular, Fibrosing pneumoconiosis
 PathogenesisPathogenesis
 crystalline forms -more fibrogenic (crystalline forms -more fibrogenic (quartzquartz ––worstworst))
 silica particlessilica particles lung macrophages ingest themlung macrophages ingest them  activation andactivation and
release of mediatorsrelease of mediators  IL-1, TNF,IL-1, TNF, oxygen-derived free radicalsoxygen-derived free radicals
 Anti-TNF monoclonal antibodies can block lung collagenAnti-TNF monoclonal antibodies can block lung collagen
accumulation in miceaccumulation in mice
 Morphology.Morphology.
• EarlyEarly stagesstages ––tiny nodules in the upper zonestiny nodules in the upper zones
• diseasedisease progressesprogresses ––nodules coalesce intonodules coalesce into hard, collagenous scarshard, collagenous scars
central softening and cavitation (due to superimposed tuberculosis orcentral softening and cavitation (due to superimposed tuberculosis or
to ischemia)to ischemia)
• X-rayX-ray –– egg shellegg shell calcification in the lymph nodescalcification in the lymph nodes
• Advanced stageAdvanced stage - PMF- PMF
 HistologyHistology
 Nodular lesions -concentric layers of hyalinized collagen surrounded by aNodular lesions -concentric layers of hyalinized collagen surrounded by a
dense capsuledense capsule

Pneumoconiosis (silicosis)

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