Skip to main content

Saturn Medic

Pneumoconiosis

Clinical Subject Page

Pneumoconiosis

Pneumoconiosis is a group of occupational lung diseases caused by long-term inhalation and accumulation of inorganic dust particles in the lungs, leading to chronic inflammation and sometimes pulmonary fibrosis.

Also called

Occupational dust lung disease

ICD-10

J62.8

Specialty

Pulmonology

Onset

Chronic

Reviewed

July 2026

On This Page

Overview

Pneumoconiosis develops after repeated exposure to harmful mineral dusts, usually in the workplace.

Major types include:

  • Silicosis → Silica dust
  • Coal workers’ pneumoconiosis (CWP) → Coal dust
  • Asbestosis → Asbestos fibers

The disease may progress from dust deposition and inflammation to permanent pulmonary fibrosis.

Etiology & Risk Factors

Main Causes

Silica Dust

Associated with:

  • Mining
  • Sandblasting
  • Stone cutting
  • Construction

Coal Dust

Associated with:

  • Coal mining

Asbestos Fibers

Associated with:

  • Construction
  • Shipbuilding
  • Insulation work
  • Demolition

Other Dusts

  • Beryllium
  • Talc
  • Iron
  • Other mineral dusts

Risk Factors

  • Long duration of exposure
  • High concentration of inhaled dust
  • Poor workplace ventilation
  • Lack of respiratory protection
  • Smoking
  • Certain high-risk occupations

Important Note

A detailed occupational history is essential in every patient with suspected pneumoconiosis.

Pathophysiology

Flow Chart

Repeated inhalation of inorganic dust
⬇
Dust deposition in the lungs
⬇
Macrophage activation
⬇
Release of inflammatory mediators
⬇
Chronic lung inflammation
⬇
Fibroblast activation + Collagen deposition
⬇
Pulmonary fibrosis
⬇
Stiff lungs + Impaired gas exchange
⬇
Progressive dyspnea and respiratory impairment

Key Concept

The type of dust determines the pattern, severity, and complications of lung disease.

Clinical Presentation

  1. Symptoms

    • Progressive exertional dyspnea
    • Chronic cough
    • Sputum production in some patients
    • Chest tightness
    • Reduced exercise tolerance

    Advanced Disease

    • Dyspnea at rest
    • Fatigue
    • Hypoxemia
    • Respiratory failure

    Signs

    • Tachypnea
    • Fine inspiratory crackles
    • Reduced oxygen saturation
    • Digital clubbing in some forms

    Advanced Signs

    • Cyanosis
    • Signs of pulmonary hypertension
    • Signs of cor pulmonale

History Taking

    • Ask about:

      • Shortness of breath?
      • Chronic cough?
      • When did symptoms start?
      • Current occupation?
      • Previous occupations?
      • Mining work?
      • Construction work?
      • Stone cutting or sandblasting?
      • Asbestos exposure?
      • Duration of exposure?

Physical Examination

  • Look for:

    • Tachypnea
    • Cyanosis
    • Reduced oxygen saturation
    • Digital clubbing

    Chest Examination

    May show:

    • Fine inspiratory crackles
    • Reduced breath sounds
    • Signs of restrictive lung disease

    Advanced Disease

    Look for:

    • Raised JVP
    • Peripheral edema
    • Signs of pulmonary hypertension
    • Signs of cor pulmonale

    Important Note

    Physical examination may be normal in early disease.

Classification

Occupational Lung Disease · Pneumoconiosis — All Types

Fibrogenic
Silica, asbestos, beryllium
Cause permanent fibrosis
Non-fibrogenic
Iron (siderosis), tin (stannosis)
Benign — no fibrosis
Latency
Months (acute) to decades
Most progress after cessation
Dx basis
Exposure + radiology
Biopsy rarely needed
1 — Silicosis Crystalline silica (SiO₂)
Exposure sources
Mining (gold, coal, tin, copper), quarrying, tunneling
Sandblasting, foundry work, stone cutting
Engineered stone countertops — up to 90% crystalline silica; highest current risk
Ceramic, pottery, glass manufacturing, construction (concrete cutting)
Types & latency
Chronic: >10 yr latency — upper lobe nodules
Accelerated: 5–10 yr — high intensity exposure
Acute: <5 yr — massive exposure; silicoproteinosis; bilateral GGO
Key complications: TB risk ×2–4 (silicotuberculosis), PMF, lung cancer (IARC Group 1), scleroderma (Erasmus), RA (Caplan), cor pulmonale
Radiology
CXRBilateral rounded nodules, upper > lower lobe, 1–10 mm. Eggshell calcification of hilar nodes (pathognomonic). PMF = large opacity ≥1 cm (ILO Cat A/B/C)
HRCTCentrilobular & subpleural nodules, perilymphatic distribution, posterior & upper predominance. Conglomerate masses (PMF). Calcified nodes.
ILORounded opacities (p/q/r). Profusion ≥1/0 required for diagnosis. Symbol ca = eggshell calcification.
PFTRestrictive (classic). Mixed or obstructive in PMF / coexisting COPD. DLCO reduced in advanced disease.
2 — Coal Worker's Pneumoconiosis (CWP) “Black Lung” Coal dust
Exposure sources
Underground coal mining — coal cutters, roof bolters, miners
Surface mining, coal preparation & processing plants
Latency typically >10–20 years
Types
Simple CWP: coal macules & nodules <1 cm — often asymptomatic, slow progression
Complicated CWP (PMF): nodules ≥1 cm — significant fibrosis, respiratory failure
Caplan syndrome: CWP + rheumatoid arthritis + large necrobiotic nodules on CXR
Key difference from silicosis: Coal macules are non-birefringent under polarized light. Emphysema (focal dust emphysema) is a characteristic feature of CWP — not typically seen in silicosis.
Radiology
CXRSmall rounded opacities (p, q, r), upper & mid zone. Simple: profusion ≥1/0. PMF: large opacities (Cat A/B/C) — bilateral, upper lobe, may cavitate. No eggshell calcification (distinguishes from silicosis)
HRCTCentrilobular nodules, focal emphysema around nodules. Conglomerate masses in PMF. Lymph node enlargement may occur.
ILORounded opacities (p/q) predominant. Profusion ≥1/0 for diagnosis.
PFTRestrictive (simple CWP). Obstructive or mixed common (focal emphysema, coexisting COPD from smoking).
3 — Asbestosis Asbestos fibres (amphibole > serpentine)
Exposure sources
Shipbuilding, ship repair — historically highest exposure
Insulation installation & removal, construction
Asbestos mining, milling, textile manufacturing
Boilermakers, plumbers, electricians, brake lining workers
Latency typically >20 years for asbestosis; >30–40 yr for mesothelioma
Asbestos-related diseases (distinct from asbestosis)
Asbestosis: diffuse interstitial pulmonary fibrosis (lower lobe)
Pleural plaques: most common manifestation; parietal pleura; benign but marker of exposure
Benign pleural effusion: earliest manifestation; exudate
Mesothelioma: malignant pleural/peritoneal tumor; latency 30–40 yr; no safe threshold
Lung cancer: synergistic risk with smoking (×50 vs. non-smoker non-exposed)
Rounded atelectasis (Blesovsky): pleural-based mass with comet tail sign
Radiology — asbestosis
CXRIrregular opacities (s, t, u) — bilateral, basal & subpleural predominance (opposite of silicosis). Pleural plaques (± calcification). Pleural thickening. Honeycombing (late).
HRCTSubpleural lines, ground-glass opacity, reticulation, traction bronchiectasis, honeycombing — lower lobe predominant. Pleural plaques diagnostic of asbestos exposure even without parenchymal fibrosis.
ILOIrregular opacities (s/t) predominant — key distinction from silicosis/CWP (rounded). Profusion ≥1/0 for asbestosis diagnosis.
PFTRestrictive — ↓FVC, ↓TLC, normal FEV₁/FVC, ↓DLCO (most sensitive early marker).
BALAsbestos bodies (>1 per mL = significant exposure). Ferruginous bodies on iron stain.
Key rule: Pleural plaques alone = asbestos exposure marker, NOT asbestosis. Asbestosis = parenchymal fibrosis. Never confuse the two — plaques do not increase cancer risk independently.
4 — Berylliosis (Chronic Beryllium Disease — CBD) Beryllium metal / alloys
Exposure sources
Aerospace & defense industries, nuclear weapons manufacturing
Electronics (semiconductors), dental alloys, fluorescent lamp manufacturing (historical)
Beryllium ceramics, X-ray tube windows, golf clubs
Even tiny exposures can cause disease in sensitized individuals (<2% of exposed workers develop CBD)
Pathophysiology & dx
Immune-mediated (Type IV hypersensitivity / delayed) — NOT a dose-response relationship. Beryllium acts as a hapten → sensitization → granulomatous inflammation. Clinically and radiologically identical to sarcoidosis — exposure history is the key differentiator.
Beryllium Lymphocyte Proliferation Test (BeLPT): Gold standard diagnostic test — peripheral blood or BAL lymphocytes proliferate in response to beryllium antigen. Positive in CBD and beryllium sensitization. Negative BeLPT excludes CBD. Not needed in other pneumoconioses.
Radiology
CXRBilateral hilar lymphadenopathy (indistinguishable from sarcoidosis). Reticulonodular opacities. Upper lobe fibrosis in advanced disease.
HRCTPerilymphatic nodules, hilar/mediastinal adenopathy, GGO, fibrosis. Identical to sarcoidosis.
BALLymphocytosis (CD4+ predominant). BeLPT on BAL cells — confirmatory.
BiopsyNon-caseating granulomas — identical to sarcoidosis. Diagnosis requires BeLPT positivity + granulomas. ACE normal or mildly elevated (vs. sarcoidosis where ACE often markedly elevated).
PFTRestrictive or mixed; reduced DLCO.
vs. Sarcoidosis: Both cause non-caseating granulomas. CBD: beryllium exposure + positive BeLPT. Sarcoid: no exposure, negative BeLPT, higher ACE, more systemic features (skin, eye, cardiac).
5 — Byssinosis “Monday fever / Brown lung” Cotton, flax, hemp, jute dust
Exposure sources
Cotton gin workers, cotton textile mills
Flax, hemp, jute processing & weaving
Highest exposure: opening room / carding room (coarsest dust)
Classic presentation — grading
Grade 0: No symptoms
Grade ½: Chest tightness & shortness of breath on first day back after break (“Monday feeling”)
Grade 1: Symptoms every Monday
Grade 2: Symptoms Monday AND other days
Grade 3: Permanent disability — chronic airflow obstruction even after cessation
Key feature: Symptoms worst on return to work after absence (Monday / first shift) — improves during the week as tolerance develops. Caused by endotoxin in dust (Gram-negative bacteria on cotton) causing bronchoconstriction.
Radiology & investigations
CXRUsually normal or non-specific. Hyperinflation in advanced disease. No nodular opacities — byssinosis is NOT a classic “nodular” pneumoconiosis.
PFTObstructive pattern (unique among pneumoconioses — most others are restrictive). FEV₁ decline across Monday shift is characteristic. Reversible early; fixed obstruction (COPD-like) in Grade 3.
DxClinical — exposure history + Monday chest tightness + obstructive spirometry. No specific biomarker or radiological finding required.
Treatment: Cessation of exposure. Bronchodilators. Grade 3 — permanent disability, managed like COPD. Antihistamines historically used (some benefit). Prevention: dust control, ventilation.
6 — Benign Pneumoconioses: Siderosis, Stannosis, Baritosis Non-fibrogenic dusts
Siderosis
Dust: Iron oxide (Fe₂O₃)
Exposure: Arc welding, iron foundries, iron ore mining, hematite mining

CXR: Dense nodular opacities (iron is radiopaque) — may appear dramatic but are benign

Key feature: No fibrosis, no functional impairment. Nodules may disappear after cessation. Welder’s lung — if coexisting silica or asbestos exposure, fibrosis can occur.

Benign — no fibrosis
Stannosis
Dust: Tin oxide (SnO₂)
Exposure: Tin mining, tin smelting, tin ore processing

CXR: Dense bilateral nodular opacities — very radiopaque (tin is dense). Striking appearance with normal or near-normal PFTs.

Key feature: No fibrosis, no symptoms, no functional impairment. Often discovered incidentally. One of the most radiologically dramatic but clinically benign pneumoconioses.

Benign — no fibrosis
Baritosis
Dust: Barium sulfate (BaSO₄)
Exposure: Barytes mining and milling, drilling mud manufacturing, rubber / paint industry

CXR: Very dense discrete nodules throughout both lung fields — extremely radiopaque. May be mistaken for metastases.

Key feature: No fibrosis, no symptoms, no functional impairment. PFTs normal. Benign incidental finding in exposed workers. Barium sulfate is inert.

Benign — no fibrosis
Type Dust Occupation CXR pattern ILO opacity PFT Key complication Fibrosis
Silicosis Crystalline SiO₂ Mining, sandblasting, stone cutting, engineered quartz Rounded nodules, upper lobe; eggshell calcification; PMF p/q/r (rounded) Restrictive TB (×4), lung cancer, PMF, scleroderma Yes — severe
CWP Coal dust Underground coal mining Rounded nodules, upper & mid zone; PMF; focal emphysema; no eggshell p/q (rounded) Restrictive / mixed PMF, focal emphysema, Caplan syndrome Yes
Asbestosis Asbestos fibres Shipbuilding, insulation, construction Irregular opacities, lower lobe; pleural plaques; honeycombing s/t (irregular) Restrictive; ↓DLCO Mesothelioma, lung cancer, pleural plaques, rounded atelectasis Yes — lower lobe
Berylliosis (CBD) Beryllium Aerospace, nuclear, electronics Hilar adenopathy; reticulonodular; identical to sarcoidosis Variable Restrictive; ↓DLCO Granulomatous fibrosis; cor pulmonale Yes — granulomatous
Byssinosis Cotton / flax / hemp dust Textile mills, cotton gins Usually normal; hyperinflation late N/A Obstructive (unique) Chronic airflow obstruction (COPD-like) Minimal
Siderosis Iron oxide Welding, iron foundries Dense nodules — radiopaque; dramatic but benign p/q (rounded) Normal None (unless mixed with silica) No
Stannosis Tin oxide Tin mining & smelting Very dense radiopaque nodules; striking but benign p/q (rounded) Normal None No
Baritosis Barium sulfate Barytes mining, drilling Very dense radiopaque nodules; may mimic metastases p (rounded) Normal None No

Investigations

  • Chest Imaging — Key Investigation

    Chest X-ray

    May show:

    • Small rounded opacities
    • Reticular changes
    • Pleural abnormalities
    • Large fibrotic masses in advanced disease

    High-Resolution CT (HRCT)

    Provides better assessment of:

    • Dust-related nodules
    • Fibrosis
    • Progressive massive fibrosis
    • Pleural disease

    Pulmonary Function Tests

    May show:

    • Restrictive pattern
    • Obstructive pattern
    • Mixed pattern
    • Reduced DLCO

    Oxygen Assessment

    • Pulse oximetry
    • Exercise oxygen testing
    • Arterial blood gas in severe disease

    Additional Tests

    Depending on the suspected type:

    • Tuberculosis testing
    • Bronchoscopy
    • Lung biopsy when the diagnosis remains uncertain

Diagnosis

Occupational Medicine · Pneumoconiosis — Diagnostic Criteria

Silicosis
Crystalline silica (SiO&sub2;)
Mining, sandblasting
Upper zones — nodular
CWP
Coal dust
Underground mining
Simple → PMF
Asbestosis
Asbestos fibres
Shipbuilding, insulation
Lower zones — fibrosis
Others
Berylliosis, Siderosis
Talcosis, Byssinosis
Dust-specific patterns
General Diagnostic Criteria — All Pneumoconioses
4 Required Pillars
✓1. Occupational exposure history — type of dust, duration, intensity, source confirmed
✓2. Adequate latency — months to decades depending on dust and dose
✓3. Characteristic imaging — CXR classified by ILO 2000; HRCT if CXR equivocal
✓4. Exclusion of mimics — TB, sarcoidosis, malignancy, HP; biopsy if uncertain
PFTs — Not required for dx but assess severity
Restrictive pattern (FVC↓, TLC↓, FEV1/FVC normal) — fibrosis predominant
DLCO reduced — sensitive early marker of parenchymal disease
Obstructive or mixed if emphysema coexists (coal dust, smoking)
ILO 2000 CXR Classification
●Profusion: 0 (none) → 3 (numerous) — subdivided 0/–, 0/0, 0/1 … 3/+
●Rounded opacities: p (<1.5 mm) / q (1.5–3 mm) / r (3–10 mm)
●Irregular opacities: s (<1.5 mm) / t (1.5–3 mm) / u (3–10 mm)
●Large opacities (PMF): A (>1 cm) / B / C — progressive massive fibrosis
●Pleural changes: plaques (site, calcification, width), diffuse thickening, effusion
Key Principles
Diagnosis is clinico-radiological — biopsy not always required
Disease is irreversible — may progress after dust cessation
Notifiable occupational disease in most countries
Silicosis Crystalline SiO&sub2;  |  Upper zones  |  Eggshell calcification
Diagnostic Criteria
Exposure: crystalline silica — mining, stone cutting, sandblasting, ceramics, glass
Imaging: bilateral upper zone rounded nodules (p/q/r) — ILO ≥1/0
Latency: chronic ≥10 yr  |  accelerated 5–10 yr  |  acute <5 yr (very high dose)
Exclusion: TB (3× increased risk — must exclude every case), sarcoidosis
Forms
Chronic simple: nodules <1 cm, upper zones, ≥10 yr latency — may be asymptomatic
Accelerated: same pattern, higher exposure, 5–10 yr
Acute (silicoproteinosis): alveolar filling pattern, BAL milky PAS+ fluid, <5 yr
PMF (Complicated): nodules coalesce >1 cm → upper zone masses, peripheral emphysema
Imaging & Histology
CXR: bilateral upper zone rounded nodules; eggshell calcification of hilar/mediastinal nodes (pathognomonic)
HRCT: centrilobular and subpleural nodules, upper lobe predominance, subpleural pseudoplaques
Histology: whorled hyalinised collagen nodule with dust-laden macrophages; birefringent silica under polarised light
Complications
Silicotuberculosis — always screen & treat TB prophylactically in high-risk regions
Lung cancer (IARC Group 1), autoimmune disease (scleroderma, RA, SLE)
Cor pulmonale in advanced PMF
Coal Worker’s Pneumoconiosis (CWP) Coal dust  |  Upper zones  |  Simple → PMF
Diagnostic Criteria
Exposure: coal dust — underground mining (hewer, ripper, driller); latency ≥10 yr
Imaging: bilateral upper zone small rounded opacities (p/q/r) ILO ≥1/0
Simple CWP: nodules <1 cm — often asymptomatic; PFTs may be normal
Complicated CWP (PMF): large opacities >1 cm (ILO A/B/C), bilateral upper zones, masses migrate toward hilum
Exclusion: sarcoidosis, TB, silicosis (may coexist in mixed dust exposure)
Caplan Syndrome
CWP + seropositive RA → multiple large peripheral nodules (0.5–5 cm), develop rapidly, may cavitate or calcify. Also occurs in silicosis & asbestosis.
Imaging & Histology
CXR simple: small rounded upper zone opacities; eggshell hilar calcification (less common than silicosis)
CXR PMF: bilateral upper zone masses, peripheral emphysema; masses migrate toward hilum over time
HRCT: centrilobular nodules, subpleural nodules, upper lobe predominance
Histology: coal macule (dust-laden macrophages, minimal collagen) → coal nodule (+ collagen) → PMF (large black fibrotic areas)
Complications
PMF, cor pulmonale, respiratory failure, COPD (emphysema from coal macules)
Caplan syndrome, moderately increased TB risk
Asbestosis Asbestos  |  Lower zones  |  Pleural plaques  |  Helsinki 2014
Helsinki 2014 Criteria (all required)
✓Interstitial fibrosis on HRCT or histology (lower zone predominant)
✓Cumulative asbestos exposure ≥25 fibre-years or ≥2 asbestos bodies/mL BAL
✓Latency ≥10 yr from first exposure (typically ≥20 yr)
✓Exclusion of other ILD causes (UIP/IPF, CTD-ILD, drug-induced)
Exposure Sources
Shipbuilding, insulation, plumbing, construction, brake linings, fire-proofing
Amphibole fibres (crocidolite, amosite) more fibrogenic & carcinogenic than serpentine (chrysotile)
Pleural plaques alone ≠ asbestosis — plaques = marker of exposure only
Imaging & Histology
CXR: bilateral lower zone irregular opacities (s/t/u) ILO ≥1/0; pleural plaques (diaphragm, lateral wall) ± calcification
HRCT (gold standard): subpleural lines, curvilinear lines, reticular pattern, traction bronchiectasis, honeycombing — basal predominant
Round atelectasis (Blesovsky): folded lung adjacent to pleural plaque
Asbestos body (hallmark): iron-coated fibre — golden-brown, beaded, drumstick shaped; Prussian blue positive
Complications
Mesothelioma (pleural/peritoneal) — amphibole predominant; long latency 30–40 yr
Lung cancer — multiplicative risk with smoking; diffuse pleural thickening, effusion
  Other Pneumoconioses
Berylliosis (CBD)
Aerospace • Nuclear • Electronics
BeLPT positive (beryllium lymphocyte proliferation test) — essential for dx
HRCT: non-caseating granulomas — indistinguishable from sarcoidosis without BeLPT
BAL lymphocytosis; BeLP test on BAL cells confirms diagnosis
BeLPT+ without disease = sensitisation only
Siderosis & Mixed Dust
Welding • Iron ore • Steel
Pure siderosis (iron oxide): benign, no fibrosis, dense nodules on CXR, normal PFTs
Silicosiderosis (iron + silica): fibrogenic, causes lung fibrosis
Welder’s lung: mixed dust (iron, manganese) — centrilobular nodules on HRCT
Others
Various occupational dusts
Talcosis: irregular opacities, upper zone; IV drug users → talc emboli
Byssinosis (cotton dust): obstructive, Monday morning tightness, FEV1 falls Monday > Friday
Baritosis (barium sulfate): dense radioopaque nodules, no fibrosis, benign
Hard metal disease (cobalt): giant cell interstitial pneumonitis (GIP) on biopsy
Feature Silicosis CWP Asbestosis Berylliosis
DustCrystalline silicaCoal dustAsbestos fibresBeryllium
Latency10–30 yr10–20 yr20–40 yrMonths–decades
ILO opacity typeRounded (p/q/r)Rounded (p/q/r)Irregular (s/t/u)Nodular / granulomatous
CXR zoneUpper > lowerUpper > lowerLower > upperUpper > lower
Pathognomonic signEggshell calcificationPMF massesAsbestos bodiesBeLPT positive
Pleural diseaseRareRarePlaques & thickeningRare
PFTRestrictive (PMF)Restrictive ± obstructiveRestrictive, DLCO↓Restrictive, DLCO↓
MalignancyLung Ca (IARC Gr1)MinimalLung Ca, MesotheliomaLung Ca (possible)
TB riskHigh (×3)ModerateLowLow
Caplan syndromeYesYes (classic)YesNo
Home / Home / Clinical Cases / Respiratory System Clinical Cases / Pneumoconiosis
Related Topics

Management

  • Main Goals

    • Stop further exposure
    • Control symptoms
    • Preserve lung function
    • Prevent complications

    Exposure Control

    • Remove or reduce further dust exposure
    • Use appropriate respiratory protection
    • Improve workplace safety

    Supportive Management

    • Smoking cessation
    • Vaccination
    • Pulmonary rehabilitation
    • Oxygen therapy when indicated
    • Bronchodilators if airflow obstruction is present

    Treat Complications

    • Respiratory infections
    • Tuberculosis when present
    • Pulmonary hypertension
    • Respiratory failure

    Advanced Disease

    • Lung transplantation may be considered in selected patients

    Important Note

    Established pulmonary fibrosis is usually irreversible; prevention and early exposure control are essential.

Complications

  • Progressive pulmonary fibrosis
  • Progressive massive fibrosis
  • Chronic hypoxemia
  • Respiratory failure
  • Pulmonary hypertension
  • Cor pulmonale
  • Tuberculosis
  • Lung cancer in some dust exposures
  • Mesothelioma with asbestos exposure
  • Death

Prognosis

  • Prognosis depends on:
    • Type of inhaled dust
    • Intensity of exposure
    • Duration of exposure
    • Extent of pulmonary fibrosis
    • Presence of complications
  • Mild disease may remain stable after exposure stops.
  • Advanced fibrotic disease may continue to progress.
  • Severe disease can lead to respiratory failure and pulmonary hypertension.
  • Prevention of further exposure is essential for improving long-term outcomes.

Key Points / Clinical Pearls

  • Pneumoconiosis is a group of occupational dust-related lung diseases.
  • Silicosis, coal workers’ pneumoconiosis, and asbestosis are major types.
  • A detailed occupational history is essential.
  • Symptoms may appear years after exposure.
  • Chest X-ray and HRCT are the main imaging tests.
  • Pulmonary function may show restrictive, obstructive, or mixed abnormalities.
  • Established fibrosis is usually irreversible.
  • Stopping further exposure is the most important intervention.
  • Silica exposure increases the risk of tuberculosis.
  • Asbestos exposure increases the risk of lung cancer and mesothelioma.