Silicosis
• Caused by prolonged inhalation of silicon dioxide,
commonly called silica. Persons at increased risk:
• Miners (e.g. of granite, sandstone, slate, coal, gold, tin
and copper), quarry workers, tunnellers, sandblasters,
grinders, ceramic workers, foundry workers and those
involved in the manufacture of abrasives containing
silica.
• Peculiar to India are the occupational exposure to pencil,
slate and agate-grinding industry carrying high risk of
silicosis (agate = very hard stone containing silica)
Pathogenesis
• Occurs after exposure for decades. Other factors, total
dose, duration of exposure, the type of silica inhaled and
individual host factors.
• Sequence of events:
• 1. Silica particles between 0.5 to 5 μm size on reaching
alveoli taken by the macrophages which undergo
necrosis.
• 2. Some silica-laden macrophages carried to respiratory
bronchioles, alveoli and in interstitial tissue. Some silica
dust transported to subpleural and interlobar lymphatics
and into regional lymph nodes
• 3. Silica dust is fibrogenic. Crystalline form, ie. quartz,
more fibrogenic than non-crystalline silica.
• 4. Activation of T and B lymphocytes, results in
increased serum levels of immunoglobulins (IgG and
IgM), antinuclear antibodies, rheumatoid factor and
circulating immune complexes as well as proliferation of
T cells.
• 5. Silica is cytotoxic and kills the macrophages which
engulf it. Released silica dust activates viable
macrophages leading to secretion of macrophage
derived growth factors as interleukin-1 that favour
fibroblast proliferation and collagen synthesis.
Morphology
• G/A:
• lung studded with well-circumscribed, hard, fibrotic
nodules, 1 to 5 mm in diameter
• Nodular lesions frequently have simultaneous deposition
• of coal-dust and may develop calcification.
• Pleura grossly thickened, adherent to chest wall.
• Nodular lesions detectable as egg-shell shadows in
chest X-rays.
• Lesions may undergo ischaemic necrosis, develop
cavitation, or complicated by tuberculosis and
rheumatoid pneumoconiosis
• M/E:
• 1. Silicotic nodules have central hyalinised material with
scanty cellularity and some amount of dust. Hyalinised centre
surrounded by concentric laminations of collagen.
• 2. On polarisation demonstrate numerous birefringent
particles of silica.
• 3. Severe and progressive form of disease result in
coalescence of adjacent nodules and cause complicated
silicosis.
• 4. Intervening lung parenchyma show hyperinflation or
emphysema.
• 5. Cavitation, complicated by tuberculosis and rheumatoid
pneumoconiosis
Asbestos disease
• Coal is lot of dust and little fibrosis, asbestos is little dust
and a lot of fibrosis.
• Three types of severe diseases:
• Asbestosis of lungs,
• Pleural disease
• Tumours.
• In nature, asbestos exists as long thin fibrils which are
fire-resistant and can be spun into yarns and fabrics
suitable for thermal and electrical insulation and has
many applications in industries
• Persons at risk are workers engaged in mining, fabrication
and manufacture of a number of products from asbestos eg.
Asbestos pipes, tiles, roofs, textiles, insulating boards, sewer
and water conduits, brake lining, clutch castings.
• Two major geometric forms of asbestos:
• Serpentine consisting of curly and flexible fibres is most
common chemical form chrysotile (white asbestos) comprising
more than 90% of commercially used asbestos.
• Amphibole consists of straight, stiff and rigid fibres and
include less common chemical forms crocidolite (blue
asbestos), amosite (brown asbestos), tremolite, anthophyllite
and actinolyte. associated with induction of malignant pleural
tumours, with crocidolite.
Pathogenesis
• 1. Inhaled asbestos fibres phagocytosed by alveolar
macrophages from where they reach the interstitium.
• 2. Asbestos-laden macrophages release chemo-attractants
for neutrophils and for more macrophages, inciting cellular
reaction around them.
• 3. Asbestos fibres coated with glycoprotein and endogenous
haemosiderin; beaded or dumbbell-shaped asbestos bodies.
• 4. All types of asbestos, fibrogenic result in interstitial fibrosis.
• 5. Few immunological abnormalities as ANA and rheumatoid
factor have been found, their role in the genesis of disease is
not clear.
• 6. Asbestos fibres are carcinogenic cause mesothelioma
C.
Morphology
• G/A:
• Lungs small and firm with cartilage-like thickening of the
pleura. C/S: Variable degree of pulmonary fibrosis, in
subpleural areas and in bases of lungs.
• M/E:
• 1. Non-specific interstitial fibrosis.
• 2. Presence of characteristic asbestos bodies in
involved areas, coating stains positively for Prussian
blue reaction.
• 3. May be changes of emphysema in pulmonary
parenchyma between the areas of interstitial fibrosis.
• Pleural Disease:
• 3 types of lesions: Pleural effusion, Visceral pleural
fibrosis, Pleural plaques
• G/A:
• Circumscribed, flat, small (upto 1 cm in diameter), firm or
hard, bilateral nodules
• M/E:
• Hyalinised collagenous tissue may calcify so that they
are visible on chest X-ray. Asbestos bodies generally not
found within the plaques.
• Tumors:
• Number of cancers, most importantly bronchogenic
carcinoma and malignant mesothelioma, others are:
carcinomas of oesophagus, stomach, colon, kidneys and larynx and
various lymphoid malignancies.
• Bronchogenic carcinoma: Incidence is 5 times higher in
non-smoker asbestos workers, 10 times higher in
smoker asbestos workers.
• Malignant mesothelioma: Association with asbestos
exposure is present in 30 to 80% of cases with
mesothelioma
