SILICOSIS
Silicosis is a chronic diffuse fibronodular interstitial lung disease caused by the inhalation of crystalline particles of silica (silicon dioxide [SiO2]). The particles must be of respirable size (0.2-10 m aerodynamic diameter) to reach the distal airspaces of the lung. The biologic activity of silica is attributable to silanol groups and other chemically reactive species on the crystal surface, not to its physical shape or sharp edges. The mineral must be in crystalline form because glass (amorphous noncrystalline silica) is essentially nontoxic in crushed, powdered, or fibrous form. The mineral silica is abundant in nature as either pure quartz or mixed in igneous rock with other minerals; whereas beach sand is pure quartz, granite contains 10% to 15% crystalline free silica. Exposure to respirable silica must be substantial and prolonged to cause clinically significant lung disease.
Silicosis usually presents as a chronic diffuse lung
disease with numerous small nodules with an upper lung zone predominance, and
it evolves slowly over years or decades. This form is labeled chronic simple
silicosis. It may progress to more extensive disease with coalescence of
the nodules into conglomerate masses with surrounding fibrosis and traction
emphysema. The more advanced stage may be referred to as progressive massive
fibrosis (PMF). Extremely high levels of expo- sure can cause an acute and
usually fatal form of silicosis accompanied by an outpouring of alveolar
surfactant lipids and proteinaceous debris, a rare condition known as acute
silicosis or silicoproteinosis. An intermediate form termed accelerated
silicosis may develop in 2 to 5 years if exposure is intense.
PATHOLOGY
The pathology of silicosis features a characteristic
lesion, the silicotic nodule, found in lung tissue and draining lymph modes.
This lesion begins as a small collection of macrophages (many containing
phagocytosed dust particles), lymphocytes, and fibroblasts; this early lesion is
usually located near respiratory bronchioles. Whorls of type I collagen and
other matrix proteins accumulate in the center as the nodules enlarge, with an
outer rim of mononuclear cells and proliferating fibroblasts. Neutrophils and
eosinophils are not abundant. The nodules coalesce gradually, and the fibrotic
process extends to infiltrate the surrounding tissue. Finally, dystrophic calcification may be found
within the larger conglomerate masses and in the hilar and mediastinal lymph
nodes. The silica mineral particles are usually abundant within these lesions
and can be visualized by polarized light microscopy or by elemental analysis
with scanning electron microscopy and energy dispersive spectrometry.
CLINICAL FEATURES
Patients with silicosis experience gradually
progressive shortness of breath with exertion and cough, sometimes with clear
or white sputum. Physical examination may be normal, or high-pitched
end-inspiratory crackles (rales) may be
heard over the mid-lung areas. Digital
clubbing is very uncommon in silicosis. Signs of cor pulmonale
(accentuated second heart sound, peripheral edema) may be late manifestations
of advanced disease. The chest radiograph early in silicosis shows small, rounded
opacities with a mid- and upper-zone pre-dominance (International Labour
Organization classification p/q opacities, profusion 1/1-2/1). More advanced
silicosis includes more widespread opacities with some coalescence, enlarged
hilar and mediastinal lymph nodes, and
peripheral “egg-shell” calcification of these nodes. Extensive pleural thickening
or pleural calcifications are not seen, although some of the nodules may originate
at subpleural sites. High-resolution (thin section) computed tomography (CT) is
helpful in revealing this pattern and may show more extensive disease than would
be suspected from the plain frontal chest radiograph. The radiographic features
of silicosis may be much more striking than either the patient’s complaints or
the pulmonary function abnormalities. Pulmonary function tests show a pattern
of mixed restrictive and obstructive physiology, commonly with oxygen
desaturation with exertion. There is no effective treatment for silicosis; it
must be prevented by industrial hygiene measures. Chronic silicosis must be
managed with supportive care, such as oxygen therapy and treatment of
intercurrent infections.
WORKPLACE EXPOSURE
Workers may be exposed to respirable silica dust in a
variety of industrial settings where the use of power machinery generates
numerous fine particles. A common theme involves drilling where the work takes
place in a confined space that may be poorly ventilated, such as through
silica-containing rock to extract minerals (mining) or stone (quarrying) or
drilling to create passageways (tunneling). Crafting stone for monuments,
tombstones, or sculpture can generate substantial airborne dust. Silica sand is
used to create abrasives, sandpaper, and grinding and polishing materials. Abrasive
blasting using sand for grit or nonsiliceous abrasive blasted against
silica-bearing stone also can cause silicosis. Sharpening tools (scissors
grinding) or cleaning sand-cast foundry parts with silica-containing abrasives
can produce substantial exposures.
Silicosis caused by mining, quarrying, tool grinding,
and similar activities can usually be reduced to safe levels by vigilant
industrial hygiene measures (air extraction, spraying water on cutting
surfaces, abrasive blasting in isolation booths, respiratory protective
devices, independent clean air sources). Workers involved in the production of
abrasives, glass sand, and particularly silica flour (finely divided silica
powder) may experience significant exposure and develop silicosis. Silica flour
is used widely as an additive, absorbent, bulking agent or an abrasive in many
products such as paints, plastics, toothpastes, and detergents. Control
measures and regulation and surveillance of exposures to silica are the major
reason for the decline in the number of cases and deaths caused by silicosis in
the United States and other industrialized nations over the past 70 years.
Silicosis is still common in developing nations where extractive industries are
growing and power equipment is being used more widely, but worker protection
and industrial hygiene remain limited. The United States Occupational Safety
& Health Administration (OSHA) and the Mine Safety Administration (MSA)
have established a Permissible Exposure Limit (PEL) for an 8-hour time-weighted
average (TWA) for crystalline quartz of less than 0.10 mg/m3; levels between
0.05 mg/m3 and 0.10 mg/m3 are specified by most nations.
SILICOTUBERCULOSIS
Patients with silicosis appear to be particularly
susceptible to a chronic indolent form of pulmonary tuberculosis. Diagnosis may
be difficult because of the silicotic radiographic changes. Complete eradication of tubercle bacilli is thought to be very
difficult, and lifelong antituberculous drug therapy is usually recommended.
CAPLAN NODULES
When silicosis or coal workers pneumoconiosis occurs
in a patient who also has rheumatoid arthritis, necrobiotic nodules (rheumatoid
nodules) may develop in the lung, a condition known as Caplan syndrome. The lesions are typically large (1.0
cm), round, and well-defined. These “Caplan nodules” often grow much more
quickly than typical silicotic nodules and may undergo central necrosis or
cavitation; they may also disappear spontaneously. The Caplan nodules are of
little clinical consequence in their own right but may raise great concern
about the possibility of tuberculosis caused by the cavitation or lung cancer
resulting from their rapid
growth.
