second most abundant element (after oxygen) in the earth’s crust. SiO 2 occurs
in either its free form or a combined state called silicate. Free silica may be in
crystalline form, such as quartz, granite, flint, and diatomite, or in noncrystalline form.
9.5.1 SILICOSIS
Silicosis is a disease caused by breathing tiny particles of crystalline free SiO 2 .
It is considered the most important of the pneumonoconiosies, or dust diseases
of the lung, not only because of its serious damaging effect on the respiratory
system but also because of the large numbers of workers throughout the world
who are at risk of contracting it. Acute silicosis is manifested within 8 to 18
months following the first exposure. Chronic silicosis may develop after a
latent period of up to 20 years. It is found among people with occupational
exposure to breathable crystalline free silica, for example in mining industries,
pottery manufacture, stone cutting and polishing, tile and clay production, and
glass manufacture. Silicosis increases susceptibility to various respiratory
infections, notably tuberculosis.
The size of the silica or silicate particles has a big effect on the degree of
tissue reaction that will occur following the inhalation of the siliceous dust.
Particles of 0.5 to 10 mm diameter are responsible for the disease because they
lead to fibrogenic reaction in alveolar tissue. Fibrous, or scar, tissue is formed,
replacing the normal lung tissue. However, the fibrous tissue does not have the
elasticity of normal tissue and so limits the lung’s ventilatory function and the
exchange of gases between the air and blood. As a result, the victim becomes
short of breath, a principal clinical characteristic of silicosis.
9.5.2 PATHOGENESIS
Many hypotheses have been advanced to explain the mode of action of silica
pertaining to its fibrogenic properties. For many years, researchers thought the
fibrogenic properties were due to the action of silicic aid (H 4 SiO 4 ). However,
Allison et al.
13 suggested that the intracellular reaction to silicic acid is the first
stage of a two-stage process in which the major fibrogenic stimulus comes from
the action of cellular enzymes rather than directly from the silicic acid itself.
According to their hypothesis, once a silica particle is arrested in the lungs, it is
invaginated leading to phagocytosis. The particle is encapsulated within the cell
in a phagosome, which soon becomes converted into a second type of lysosome
(digestive vacuole) through merging with a primary lysosome, presumably
secreted by the Golgi body. Protective substances adsorbed onto the silica
particles (e.g., plasma proteins) are stripped off by the enzymes released from
the lysosome, exposing silicic acid. The highly reactive silicic acid acts as a
hydrogen donor, forming hydrogen-bonded complexes with active groups of
the lipid membrane, such as phosphate ester groups, and with secondary amide
(peptide) groups of proteins. This reaction causes the lysosomal membrane to
become permeable, allowing its enzymes to leak into the cytoplasm and destroy
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in either its free form or a combined state called silicate. Free silica may be in
crystalline form, such as quartz, granite, flint, and diatomite, or in noncrystalline form.
9.5.1 SILICOSIS
Silicosis is a disease caused by breathing tiny particles of crystalline free SiO 2 .
It is considered the most important of the pneumonoconiosies, or dust diseases
of the lung, not only because of its serious damaging effect on the respiratory
system but also because of the large numbers of workers throughout the world
who are at risk of contracting it. Acute silicosis is manifested within 8 to 18
months following the first exposure. Chronic silicosis may develop after a
latent period of up to 20 years. It is found among people with occupational
exposure to breathable crystalline free silica, for example in mining industries,
pottery manufacture, stone cutting and polishing, tile and clay production, and
glass manufacture. Silicosis increases susceptibility to various respiratory
infections, notably tuberculosis.
The size of the silica or silicate particles has a big effect on the degree of
tissue reaction that will occur following the inhalation of the siliceous dust.
Particles of 0.5 to 10 mm diameter are responsible for the disease because they
lead to fibrogenic reaction in alveolar tissue. Fibrous, or scar, tissue is formed,
replacing the normal lung tissue. However, the fibrous tissue does not have the
elasticity of normal tissue and so limits the lung’s ventilatory function and the
exchange of gases between the air and blood. As a result, the victim becomes
short of breath, a principal clinical characteristic of silicosis.
9.5.2 PATHOGENESIS
Many hypotheses have been advanced to explain the mode of action of silica
pertaining to its fibrogenic properties. For many years, researchers thought the
fibrogenic properties were due to the action of silicic aid (H 4 SiO 4 ). However,
Allison et al.
13 suggested that the intracellular reaction to silicic acid is the first
stage of a two-stage process in which the major fibrogenic stimulus comes from
the action of cellular enzymes rather than directly from the silicic acid itself.
According to their hypothesis, once a silica particle is arrested in the lungs, it is
invaginated leading to phagocytosis. The particle is encapsulated within the cell
in a phagosome, which soon becomes converted into a second type of lysosome
(digestive vacuole) through merging with a primary lysosome, presumably
secreted by the Golgi body. Protective substances adsorbed onto the silica
particles (e.g., plasma proteins) are stripped off by the enzymes released from
the lysosome, exposing silicic acid. The highly reactive silicic acid acts as a
hydrogen donor, forming hydrogen-bonded complexes with active groups of
the lipid membrane, such as phosphate ester groups, and with secondary amide
(peptide) groups of proteins. This reaction causes the lysosomal membrane to
become permeable, allowing its enzymes to leak into the cytoplasm and destroy
Air Pollution – Particulate Matter
139
[16:52 26/8/04 P:/CRC PRESS/4365 MING-HO.751 (1670)/4365-009.3d]
Ref: 4365 MING-HO YU Chap-009 Page: 139 135-148