Pathology of Occupational Lung Diseases and Pneumoconiosis
Pneumoconiosis
lung disease caused by the inhalation of dust, usually occupationally related. Dependent on:
(1) the amount of dust retained in the lung and airways
(2) the size, shape, and therefore buoyancy of the particles
(3) particle solubility and physiochemical reactivity
(4) the possible additional effects of other irritants (e.g., concomitant tobacco smoking).
Coal Worker's Pneumoconiosis (CWP)
(1) Anthracotic pneumoconiosis
("black lung disease")
Characterized by the inhalation and deposition of black, carbonaceous pigment in the lung.
Carbon, derived from coal dust, in its pure form, is minimally fibrogenic.
silica (SiO2) is an irritant so those digging in a central vein are at less risk than those tunneling through silica rock.
Development of pulmonary disease depends upon the particle size and the level at which it is deposited within lung.
Particles greater than 10 m m are filtered in the nasal passages
Particles between 2 and 10 m m reach the airways and are filtered by the mucociliary escalator
Particles 0.5 to 2 m m reach alveoli and are slowly cleared by macrophages, which migrate to airways or lymphatics.
(2) Coal worker's pneumoconiosis
: occurs when macrophage clearance mechanism is overwhelmed – more dust is deposited than can be removed.
Simple CWP
characteristic lesions:
Coal
macules (1-2 mm) is the primary lesion of coal workers pneumoconiosis due to incorporation of carbon filled macrophages into walls of alveoli adjacent to respiratory bronchioles and alveolar ducts, site of dust accumulation.
Focal emphysema =
deposition of carbon in the respiratory bronchioles that produces bronchiolar dilatation
Centrilobular emphysema
produces more extensive dilation of airways, extends further beyond the bronchiole and is associated with alveolar septal destruction fine reticulin fibers and no collagen.
Complicated CWP
: Progressive massive fibrosis (PMF)
Coal nodules
:micronodular (>2< 7 mm in diameter) and macronodular (> 7 mm) forms.
collagen is formed within macules Þ firm, palpable nodules which are deeply pigmented and irregular
contrasted to Silicotic nodules which tend to be less pigmented and have a more regular, rounded shape
fibrotic nodule filled with necrotic black fluid
results in bronchiectasis, pulmonary HTN, or death from respiratory failure or right sided heart failure.
always seen in a background of simple coal worker's pneumoconiosis.
Pathogenesis of the nodular lesions of CWP
Silica is probably important in converting a macule to a nodular lesion
TB was once thought to be important but is no questioned.
Immunological factors are often found to be elevated: anti-nuclear antibodies and lung reactive antibodies
Caplan's syndrome:
coexistence of rheumatoid arthritis with a pneumoconiosis, leading to the development of distinctive Caplan's nodules which tend to be less pigmented than typical PMF, are large and many contain necrobiotic rheumatoid nodules at their periphery that develop fairly rapidly
Disruptive emphysema can coexist but no evidence exists proving this is a causative agent.
Silicosis
caused by the inhalation of crystalline silica (SiO2). Exposures include mining (i.e. gold, copper), quarrying of granite and sandstone, stone masonry and metal grinding, casting and sandblasting
Initiated by ingestion of silica dust (1-3
m m in diameter) by macrophages and localized within the phago-lysosome
silica causes the lysosome to rupture resulting in cell death and release of both the silica and lysosomal enzymes.
Lysosomal enzymes
Þ inflammatory response Þ a cellular nodule within the pulmonary interstitium Þ hyalinizes with time
Micro
: simple silicotic nodules are composed of dense collagen arranged in whorles.
crystals can been seen within the lesion with polarized light.
Distinct from PMF by regular borders and less dark pigment.
silicotic nodules can enlarge, eventually obstructing airways and blood vessels and
Þ pulmonary hypertension.
Eggshell calcification of hilar lymph nodes may be detected on chest x-ray.
Silicotuberculosis
refers to the increased susceptibility to TB associated with silicosis.
Caplans syndrome
may also occur.
Asbestos Related Disease
Asbestosis
caused by the inhalation of asbestos fibers (fibrous ciliates) which can be either the serpentines (crysotile) consisting of long, tortuous fibers, and the amphiboles (crocidolite and amosite), which are straight, rod-like fibers.
initiated by uptake of asbestos fibers by alveolar macrophages. A fibroblastic response occurs, probably from release of fibroblast-stimulating growth factors by macrophages, leads to diffuse interstitial fibrosis, mostly in lower lobes.
Is characterized by ferruginous bodies, yellow-brown, rod-shaped bodies with clubbed ends that stain positively with Prussian blue; these arise from iron and protein coating on fibers.
Pleural Disease due to asbestos exposure
Dense scalloped hyalinized fibrocalcific pleural plaques of the parietal pleura are also present.
Pleural
calcification frequently develops more than 20 years following initial exposure. Detected by routine CXR
Results in Ý risk of broncogenic carcinoma and malignant mesothelioma of the pleura or peritoneum. Cigarette smoking further Ý the risk of bronchogenic carcinoma.