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Pathology
Lecture 34 Pneumoconioses
1) Summarize the major factors in pneumoconiosis development and lung defense
mechanisms in terms of particle size and site of deposition of inhaled dust.
Factors in Pneumoconiosis Development
Amount of dust retained in the lung
size and shape of the dust particles
solubility and chemical reactivity of dust particles
presence of other irritants (cigarettes) or diseases
Lung defense mechanisms
Filtration and impaction in the upper respiratory tract
Cough
Mucociliary transport
Phagocytosis and transport by macrophages
2) Distinguish the various morphologic patterns of lung injury from dusts and give
examples.
Type of dust
Mineral
Mineral
Mineral
Mineral
Organic
Lung reaction
Accumulation in macrophages; no appreciable fibrosis
Sarcoid like granulomas
Nodular or massive fibrosis
Diffuse interstitial fibrosis (fibrosing alveolitis)
Allergic alveolitis
Examples
Iron, barium
Beryllium
Quartz (silica), coal
Asbestos
Fungal spores, avian proteins
3) Compare and contrast the mild and severe lesions of coal, silica, and asbestos
exposure.
Mild coal: Simple CWP small aggregates of dust laden macrophages.
Severe coal: Complicated Coal Workers Pneumoconiosis also called Progressive
Massive Fibrosis (PMF) <10% simple CWP become PMF.
Mild silica: Nodular (Chronic) Silicosis presents with few symptoms, 1-5 mm
parenchymal nodules consisting of layers of relatively a cellular fibrous tissue.
Severe silica: Acute Silicosis is an uncommon disease characterized by large numbers
of silica particles in alveoli associated with large amounts of proteinaceous debris.
PNF may result from coalescence of smaller silica nodules into large fibrous masses.
Mild asbestos: localized fibrous plaques, diffuse pleural fibrosis, pleural effusions,
and parenchymal interstitial fibrosis.
Severe asbestos: lung carcinoma, mesotheliomas, and laryngeal (also
extrapulmonary) neoplasms
4) Discuss coal workers pneumoconiosis, silicosis, berylliosis, and asbestos exposure
in terms of major clinical associations, gross and microscopic pathology and
associations with other diseases.
Disease
Coal Workers
Pneumoconiosis
(CWP)
Silicosis
Berylliosis
Asbestos
Exposure –
Two forms
serpentine and
amphibole
(↑pathogenic)
Clinical Associations
Little or no functional
impairment
Most prevalent chronic
occupational disease.
Silica produces free
radicals, damaging
macrophages to release
cytokines (inflammation)
Type IV cellular immune
response
(hypersensitivity) forms
granulomas
Dyspnea and cough.
Fibrogenic, asbestos
fibers are phagocytized
causing the release of
chemical mediators
resulting in fibrosis.
Gross
Fibrous nodules >2 cm with
black pigment in upper
lobes
1-5 mm nodules in upper
lobes of lungs
Microscopic
Dense collagen and
pigment with necrotic
center
Nodular lesions of
concentric layers of
hyalinized collagen
with a dense capsule
Disease Associations
Anthracosis (any black
dust accumulation)
Tuberculosis
PMF - right heart failure,
tuberculosis, Caplan's
Usually no demonstrable
alteration, although
coalescence of granulomas
may produce small nodules
Pleural plaques of dense
collagen develop on the
anterior and posterolateral
aspects of the parietal pleura
and over the domes of the
diaphragm.
Granulomatous
disease virtually
identical to
sarcoidosis
Asbestos bodies,
golden brown,
fusiform or beaded
rods consisting of
asbestos fibers coated
with iron and proteins
Increased risk of lung
cancer, HLA-DPβ-Glu69
allele confers greater risk
to those exposed.
Lung cancers, potentiates
the effects of smoking,
50-80% of all diffuse
mesotheliomas.