the lung resulting from exposure to organic and inorganic
particulates, most commonly mineral dust
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? Pathogenesis-
(1) amount of dust
(2) size, shape, and buoyancy of the particles
osmall particles,1 to 5 m ?acute lung injury
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oLarge particle-evoke fibrosing collagenous pneumoconioses
(3) particle solubility and physiochemical reactivity-small particles composed of
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injurious substances of high solubility(4) additional effects of other irritants
? particles stimulate resident innate immune cells in the lung
? invokes systemic response
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? a genetic predisposition
Particles size
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?2.5?10 m-? bronchi and bronchioles
? removed by mucociliary action
? <2.5 m- acini
?<100 nm-penetrate alveolar walls
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Silicosis
? Silicosis is the most common pneumoconiosis in the world, and
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crystalline silica (e.g., quartz) is the usual culprit
? caused by inhalation of proinflammatory crystal ine silicon dioxide
Pathogenesis-
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?crystalline and amorphous forms? crystalline forms (including quartz, cristobalite, and tridymite)- much more
fibrogenic
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? Phagocytosed silica crystals activate the inflammasome, leading to the release ofinflammatory mediators, particularly IL-1 and IL-18
? disease may continue to worsen even if the patient is no longer
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exposed
? It is associated with an increased susceptibility to tuberculosis
? Patients with silicosis have double the risk for developing lung cancer
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?SIMPLE NODULAR SILICOSIS: most common form of silicosis?PROGRESSIVE MASSIVE FIBROSIS: nodular masses greater than 2 cm
in diameter, in a background of simple silicosis
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? bilateral? 5?10 cm
? Central cavitation
?ACUTE SILICOSIS:
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? heavy exposure to finely particulate silica during sandblasting or boiler scaling? it is associated with diffuse fibrosis of the lung
? Silicotic nodules are not found
? Microscopically,Dense eosinophilic material accumulates in alveolar spaces
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Gross
Progressive massive fibrosis
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Several coalescent collagenous silicotic nodules
Coal Workers' Pneumoconiosis
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? caused by inhalation of coal particles and other admixed forms ofdust
? Contaminating silica in the coal dust favour progressive disease
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? develop emphysema and chronic bronchitis independent of smokingMORPHOLOGY
? Anthracosis is the most innocuous coal-induced pulmonary lesion in coal miners
?coal macules (1 to 2 mm in diameter) and somewhat larger coal nodules
? Coal macules consist of carbon-laden macrophages
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? Complication- centrilobular emphysema?Complicated coal workers' pneumoconiosis (progressive massive fibrosis)
? intensely blackened multiple scars 1 cm or larger
? Microscopy- dense collagen, pigment ,+/- necrosis
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? Caplan syndrome- combination of rheumatoid arthritis (RA) and pneumoconiosis
that manifests as intrapulmonary nodules, which appear homogenous and well-
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defined on chest X-ray.? Nodular lesions are large (1?10 cm), multiple, bilateral
? Caplan nodule- combination of silicotic and rheumatoid nodule
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Asbestos-Related Diseases
? Asbestos (Greek, "unquenchable") includes a group of fibrous silicate minerals
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that occur as thin fibers
? Chrysotile accounts for the bulk of commercially used asbestos
? The amphiboles include amosite, crocidolite, tremolite, actinolite and
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anthophyllite.
? ASBESTOSIS: Asbestosis is diffuse interstitial fibrosis resulting from
inhalation of asbestos fibers
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? historically seen in asbestos miners, millers and insulators
ETIOLOGIC FACTORS:
? Asbestos fibers may be long (up to 100 m) but thin (0.5?1 m), so
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their aerodynamic particle diameter is small
? They deposit in distal airways and alveoli, particularly at bifurcations
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of alveolar ducts? first lesion is an alveolitis
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PATHOLOGY:? bilateral, diffuse interstitial fibrosis
? asbestos bodies in the lung In early stages, fibrosis
? end-stage or "honeycomb" lung
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AsbestosisAsbestos bodies
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Pleural plaque? BENIGN PLEURAL EFFUSION
? PLEURAL PLAQUES-
?most common manifestation of asbestos
?well-circumscribed plaques of dense collagen often calcified
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? DIFFUSE PLEURAL FIBROSIS? ROUNDED ATELECTASIS
? MESOTHELIOMA
? CARCINOMA OF THE LUNG
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Beryl iosis? pulmonary disease that follows the inhalation of beryllium
? materials in aerospace, industrial ceramics and nuclear industries
Pathology
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? Acute chemical pneumonitis or a chronic pneumoconiosis
? 10% progress to chronic disease, Chronic berylliosis
? Exposure may be minimal and brief
? Microscopical y, Multiple noncaseating granulomas are distributed
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along the pleura, septa and bronchovascular bundles
? may progress to end-stage fibrosis and honeycomb lung
? associated with an increased risk of lung cancer
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Beryl iosis
Talcosis
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? Prolonged and Heavy Exposure to Talc Dust
? magnesium silicates
? lubricants, and in cosmetics and pharmaceuticals
? Associated minerals such as silica may contribute to the fibrotic
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changes
? Tiny nodules to severe fibrosis
? Foreign body granulomas associated with birefringent plate-like talc
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particles
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