Pathologic Diagnosis in Occupational Lung Diseases

Dr.E.Handan ZerenÇukurova University

Occupational lung disease ≠ Pneumoconiosis

Pneumoconiosis = Retention of and pathologic effects from the inhalation of dust particles

Many of the diseases named occupational lung disease do not match with this definition

In most cases, the diagnoses is made without tissue examination…. History of the patient Clinical findings Radiologic features Epidemiologic features

Properties of inhaled dust particles… Size (Particles <10μm and more

likely <5μm reach the lung parenchyma)

Fibers, esp. asbest can reach the parenchyma when larger than 10 μm.Width is an important factor

Chemical properties

Mineralogic propertiesall affect the potency of a dust particle to cause lung injury

Pathologic reaction patterns Fibrogenic particles (asbestos,

silica) Nodular fibrosis Intersititial fibrosis Both

Non-Fibrogenic particles (carbon)

Centriacinar emphysema Centriacinar dust macules Mineral dust airway disease Dust-laden macrophages along lymphatic

routes- bronchovascular bundles, pleura, interlobular septa

Noduler fibrosis Diffuse interstitial fibrosis- UIP Massive fibrosis Other reactions- granulomatous reaction,

alveolar proteinosis, hipersensitivity pneumonitis etc.

Hyaline pleural plaques

Pleuritis and pleural fibrosis

Coal Worker’s Pneumoconiosis(CWP) The most significant factor in the

development of CWP is the cumulative exposure to coal dust

Simple CWP- Macules of coal dust and focal emphysema (centriacinar- similar to smoker’s emphysema)

CWP: Different pathologic patterns

Coal nodules

Rheumatoid pneumoconiosis Progressive massive fibrosis

Silicosis

Nodular fibrosis < 10 mm- simple silicosis >1 cm- complicated silicosis

At least a latent period of 20 years Accelerated silicosis- A latent period

of 3-10 years

Dr.Andrew Churg- Van Couver, Canada

Acute Silicoproteinosis

Same morphology with alveolar proteinosis

Heavy silica inhalation Symptomatic within 3 years, fatal

in most cases

Early Silicosis

Formation of the silicotic nodule

PMF (Progressive massive fibrosis) in silicosis If necrosis is present, TB must be

roled out

Mixed dust pneumoconiosis

İsolated pleural silicosis

ZEREN EH, COLBY TV, ROGGLI VL. SILICA-INDUCED PLEURAL DISEASE: AN UNUSUAL CASE MIMICKING MALIGNANT MESOTHELIOMA. CHEST (1997)112:1436-8

Diseasesassociated with Asbestos exposure Asbestosis Asbestos airway disease Non-neoplastic pleural patologic

conditions Benign asbestos effusion Visseral pleural fibrosis Hyaline pleral plaque

Lung cancer Malignant mesothelioma

Asbestos bodies

Ghio AJ, Churg A, Roggli VL; Toxicologic Pathology (2004)32:643-649

Asbestosis Heavy exposure, latent period ↓ Pleural involvement- an important

clue Involvement of the lower lobes

Pulmonary Siderosis Deposition of iron and iron oxides following

the exposure- not very uncommon No clinically apparent disease unless mixed

with other fibrogenic dusts Small airway dysfunction and emphysema if

inhaled in large amounts

Asbestosis + Siderosis

Berilliosis-chronic berillium disease Metal working, ceramic, electronic,

computer industry, space industry, dental laboratories using berillium alloys, florescent lamp manufacturing

Multisystemic disease Similar clinic and pathologic features

with sarcoidosis

Hard metal (Cobalt) lung disease As hard as dimond- ideal for ctting

of metal tools Formerly, categorized as “Giant

cell intersititial pneumonia” in Leibow’s classification

Occupational hipersensitivity pneumonia (HP) (extrinsic allergic alveolitis) Organic antigens or simple

inorganic chemical compounds The exposure is obvious in most

cases (e.g: Farmer’s lung); whereas it can be difficult to identify in some others (e.g: Contamination of ventilation system)

Hot-tub disease- Water supplies contaminated by M.Avium

HP

Type 3 (immune complex) ve Type 4 (T-cell mediated, delayed type hypersensitivity ) immune reactions

Acute- 4-6 hours Subacute- days-weeks Chronic- long lasting, low amounts

of antigen exposure. Irreversible respiratory function disability and fibrosis can occur

HP-Histology

Chronic bronchiolitis + peribronchiolar interstitial pneumonia

Lyphocytic + histiocytic inflammation, rare eosinophils and plasma cells

Loose granulomas in 2/3 of cases

HP

Fibroblastic plugs filling the alveol lumens (Masson bodies)

In old cases, irreversible changes such as UIP features and end stage lung- difficult to diagnose

Differential diagnosis-HP

Collagen vascular diseases, drug reactions, infections, NSIP

DETAILED CLINICAL INFORMATION + SPECIAL STAINS FOR MICROORGANISMS +IDENTIFICATION OF THE RESPONSIBLE ANTIGEN

Organic dust toxic syndrome Acute, systemic illness following massive

exposure to organic dusts containing microorganisms or their endotoxins

Farmers exposed to grains or moldy hay contaminated with fungi

Not a real immune reaction as it occurs without prior history of sensitization

Intraalveolar space- neutrophils and histiocytes

Acute bronchiolitis

Gases and Fumes

ARDS Chronic bronchitis Necrotizing bronchiolitis Asthma Bronchiectasis Organizing pneumonia

Conclusions

The diagnosis of occupational and environmental diseases is made by combining the clinical, epidemiological, radiologic, and pathologic features with the patient’s occupational and environmental status

In the diagnosis, these questions are important: Is there a clear evidence of exposure to a

known agent that is associated with the findings identified?

How strong is this association and chance of developing the disease?

What is the temporal sequence ofthe exposure, and the onset of the disease?

Can the pathologic findings be explained only by the exposure?

Is the exposure related to a single disease?

THANK YOU…