Diagram showing Pathogenesis of Pneumoconiosis
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Pneumoconiosis
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Asbestosis
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Coal Pneumoconiosis
;
Talcosis.
Silicosis is caused by the inhalation
of silicon dioxide, of which there are three molecular configurations.
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The most important is quartz, and the others are crystobalite and
trydimite.
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The earth’s crust is composed largely
of silicon and its oxides, and these often combine with other minerals
to form silicates.
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Silicone granulomas
Silicon dioxide, often referred to as
“free silica”, has the distinction of producing the best-known and the
most widespread pneumoconiosis.
Silicosis is acquired in
sandblasting. Mining also involves exposure to silica, as do numerous
other occupations, including stone cutting, polishing and sharpening
of metals, ceramic manufacturing, foundry work, and the cleaning of
boilers.
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Emphysema and airway obstruction in non-smoking South African gold
miners with long exposure to silica dust.Occup
Environ Med. 1994 Aug;51(8):557-63
OBJECTIVE--Occupational exposure to silica dust is associated with
significant impairment of lung function. The present study
investigates which pathological changes in the lung are associated
with impairment of lung function in silica dust exposed workers
who were life-long non-smokers. METHODS--242 South African white
gold miners who were lifelong non-smokers and who had a necropsy
at death were studied. The pathological features identified at
necropsy were the degree and type of emphysema, the presence of
airway disease, and the degree of silicosis in the lung parenchyma
and pleura. These features were related to lung function tests
done a few years before death, to type of impairment (obstructive
or restrictive), and to cumulative silica dust exposure.
RESULTS--The degree of emphysema found at necropsy was not
associated with a statistically significant impairment of lung
function or with dust exposure. The degree of silicosis in the
lung parenchyma and the large airways disease (based on mucus
gland hyperplasia) were associated with a statistically
significant impairment of lung function. The large airway disease
was, however, not positively associated with dust exposure or
silicosis. In miners with a moderate or a higher degree of
limitation of airflow the main findings were silicosis, heart
disease, and obesity. The presence of small airways disease could
not be established from the necropsy material. CONCLUSION--The
results indicate that the level of exposure to silica dust to
which these miners were exposed, without a confounding effect of
tobacco smoking, is not associated with a degree of emphysema that
would cause a statistically significant impairment of lung
function. Silicosis of the lung parenchyma was associated with
loss of lung function. Other factors that may play a part in
impairment of lung function in these miners are obesity and heart
disease.
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Simple Nodular
Silicosis:
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Simple nodular silicosis is the most
common form of silicosis and is almost inevitable in any worker
chronically exposed to silica.
The lungs contain silicotic nodules
(always less than 1 cm in diameter, and usually 2 mm to 4 mm in
diameter) that, on histologic examination, have a characteristic
whorled appearance, with concentrically arranged collagen that forms
the largest part of the nodule.
At the periphery there are aggregates
of mononuclear cells, mostly lymphocytes, and fibroblasts.
Polarized
light reveals doubly refractile silicates within the nodule, but these
are not related to the pathogenesis of silicosis (only free silica is
responsible).
Hilar nodes become enlarged and
calcified, often at the periphery of the node (“eggshell
calcification”).
It has now become apparent that simple
silicosis is not usually associated with significant disability, as
assessed by pulmonary function.
Progressive
Massive Fibrosis:
Progressive massive fibrosis (PMF) is
defined radiologically as nodular masses of more than 1 cm diameter in
a background of simple silicosis.
Most of these lesions are
considerably large (about 5-10 cm in diameter) and are usually
located in the upper zones of the lung.
Morphologically, the lesions
often exhibit central necrosis, although in some instances they
consist of aggregates of nodules of simple silicosis (“conglomerate
silicosis” ).
It is well recognized that tuberculosis is much more
common in patients with silicosis than in others and that it is a
serious complication. This complication was first described in South
Africa . Most of
the gold miners there are migrant workers who are employed on a
short-term contract. Lesions of tuberculosis in
the miners closely resemble PMF, hence the notion that PMF is due to
tuberculosis.
Most observers give less importance to
the tuberculous theory of PMF now than was once the case.
Progressive massive fibrosis is related
to the amount of silica in the lung.
Disability is caused by the destruction
of lung tissue that has been incorporated into the nodules.
Acute silicosis:
Now uncommon, acute silicosis results
from heavy exposure to finely particulate silica during sand blasting
or boiler scaling.
It is associated with diffuse fibrosis of the lung
in which classic silicotic nodules are not found.
Dense eosinophilic
material accumulates in the alveolar spaces to produce an appearance
that resembles alveolar lipoproteinosis.
Indeed, experimental
administration of finely particulate silica has been used as a model
for that condition.
The disease progresses rapidly over a few years,
in contrast to other forms of silicosis, the progression of which is
measured in decades.
On radiologic examination, acute
silicosis shows diffuse linear fibrosis and a reduction in lung
volume.
Clinically, there is a severe
restrictive defect.
Etiology and
Pathogenesis:
It was originally thought that the
varying degrees of fibrosis associated with different forms of silica
reflected differing solubilities.
The popular view today is that
following the ingestion of silica, macrophages produce a
fibroblast-stimulating factor.
Because of the toxicity of silica, the
macrophage dies, thereby releasing the ingested silica and the
fibroblast-stimulating factor.
The silica is then reingested by
macrophages and the process is amplified.
The cytotoxicity of silica
results from the contact between the mineral particle and the target
macrophages.
For many years, the death of these cells has been related
to the fate of the particles after this contact.
In particular, the
release of lysosomal enzymes into the cytosol follows rapidly on the
phagocytosis of silica particles.
It has been suggested that the
breakdown of cellular components as a result of the release of lysosomal components produces irreversible cell injury.
Although
intracellular lysosomal rupture has been documented in silica-treated
macrophages, the evidence that it causes cell death is only
circumstantial.
Experimentally, it has been possible to dissociate
intracellular lysosomal rupture from cell death after exposure to
silica particles.
It is likely that the macrophages are killed because
of direct damage to the plasma membrane.
Immunologic mechanisms may
also be involved in the pathogenesis of silicosis.
Immunoglobulins are
present in the silicotic nodules, and abnormal serum immunoglobulins
(Eg. antinuclear antibodies) are also often present.
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