PNEUMOCONIOSIS CAUSED BY VARIOUS MINERALS AND MIXED DUSTS
Numerous minerals and metals that are mined, milled, quarried, carved, or used in industrial processes can cause lung disease if particles or fumes are inhaled. In many instances, the materials are relatively inert. Large amounts of the mineral can accumulate in the lung to create an impressive dust burden on pathologic examination (iron) or a striking chest radiograph (barium) but few symptoms and little pulmonary dysfunction. In some instances, metal fumes (cadmium) or particles (cobalt) can cause acute lung injury or trigger an immune response.
KAOLIN
China clay (kaolin, aluminum silicate) is mined from
surface quarries and crushed to a fine powder. Kaolin is used widely as an
absorbent, as an additive to thicken paints and other products, and to
manufacture porcelain ceramics. Workers exposed to high levels of kaolin dust
may accumulate large amounts of the mineral in their lungs and may develop a
mild pneumoconiosis that resembles silicosis.
MIXED-DUST PNEUMOCONIOSIS
Mixtures of various minerals comprise most naturally
occurring stone. When stone or earth is excavated, blasted, crushed, or
crafted, the airborne dust contains a mixture of crystalline and amorphous
minerals that reflect the source. If dust exposure is intense or pro- longed,
these minerals accumulate in the lungs of exposed workers and may be evident
either as a “storage disease” or as overt pulmonary fibrosis. The extent of lung
disease depends primarily on the fraction of crystalline free silica present in
the mixed dust and the pathogenicity of other silicates (e.g., aluminum
silicates, magnesium silicates).
COBALT PNEUMOCONIOSIS (HARD METAL DISEASE)
Cobalt exposure is associated with interstitial lung
disease and occupational asthma. These diseases occur only in occupational
settings, and there is no indication that cobalt metal or cobalt compounds
constitute a health risk for the general population. The interstitial lung
disease develops only when the exposure to cobalt occurs in association with
tungsten carbide (known as “hard metal”) or with diamond dust. This specific
pneumoconiosis is known as “hard metal disease.” Only a small fraction of
exposed workers develop the disease, and the mechanisms appear to be
immunologic sensitization rather than (or in addition to) direct lung injury.
The clinical features of cobalt pneumoconiosis are variable and include a
subacute form with rapidly progressive cough, fever, and shortness of breath as
well as a more chronic form with gradually progressive respiratory impairment.
Chest radiograph patterns vary from patchy infiltrates to diffuse small nodular
infiltrates or reticulonodular
opacities. The pathology of cobalt pneumoconiosis is distinctive, and the hallmark
features are bizarre giant cells in association with a pattern resembling
“usual interstitial pneumonitis” or “desquamative interstitial pneumonitis.” A
picture similar to that of hypersensitivity pneumonitis can be seen in the
subacute form.
The adverse responses to cobalt in the lung appear to
be primarily immunologic but may also involve direct injury or toxicity. Cobalt can be detected in
the urine of exposed workers. Cobalt may or may not be detected in lung biopsy
specimens of patients with cobalt pneumoconiosis. Cobalt can cause asthma and
contact dermatitis associated with IgE antibodies and possibly T-cell–mediated
responses against cobalt. The granulomatous “giant cell interstitial
pneumonitis” characteristic of hard metal disease includes abundant lymphocytes and
macrophages, particularly in the earlier or subacute form.
Cobalt metal is used to sinter, cement, or fuse dis-
similar materials when the mixture is heated together. In this application,
cobalt is used widely to create “hard metal” coatings on steel tools and parts
and abrasives in which tungsten carbide particles or diamond-cobalt particles
are applied to disks or wheels for grinding tools. Workers who produce tools or
parts coated with hard metal for durability and workers manufacturing tungsten
carbide or diamond abrasives are at risk for developing cobalt pneumoconiosis.
Individuals who later use these abrasives or who sharpen tools with tungsten
carbide tips are also at risk.
CADMIUM
Cadmium is an element that occurs as a soft bluish-
white metal, usually refined as a byproduct of smelting other metals such as
zinc. It is used for pigment (cadmium yellow), batteries, and other chemical
applications. The use of cadmium is sharply limited by its high toxicity and carcinogenicity.
Workers can inhale cadmium from the smelting and refining of metals, from the
air in plants that make cadmium products, or when soldering or welding metal
that contains cadmium. Acute exposure to cadmium fumes may cause flulike
symptoms, including chills, fever, and muscle aches. More severe exposures can
cause tracheobronchitis, pneumonitis, and pulmonary edema. Symptoms of
inflammation may start hours after the exposure and include cough, dryness and
irritation of the nose and throat, headache, dizziness, weakness, fever,
chills, and chest pain. Inhaling cadmium-laden dust quickly leads to
respiratory tract and kidney injuries that can be fatal.
FULLER EARTH
“Fuller earth” (magnesium oxide, calcium
montmorillonite, attapulgite, calcium bentonite) is fine clay used to absorb
oils from wool, friction pads, and other materials. Exposure during the mining
or milling of Fuller earth may cause the accumulation of large amounts of the
clay in the lungs. The mineral may be contaminated with silica, calcite,
dolomite, or other materials. The lung disease is likely caused by quartz and
other silicates that contaminate the magnesium oxide.
GRAPHITE
Graphite mineral is pure carbon, a form of highly
compressed coal, and is sometimes referred to as meta-anthracite. It is mined
from ore deposits and is used for the “lead” in pencils, as a lubricant, and to
compose electrodes. Workers exposed to airborne graphite in mining, milling, or
manufacturing may accumulate large amounts of the mineral in their lungs. It
resides mostly in the macrophages that ingest it and in the regional lymph
nodes where they transport it. Although impressive on pathologic examination,
it causes little pulmonary
dysfunction. Graphite lung disease might be considered a variant of coal worker’s pneumoconiosis caused by a very pure form of coal.
SIDEROSIS
Inhalation of iron ore dust (iron oxide) causes
accumulation of the brick-red pigment in the macrophages and lymphatic
structures of the lung (i.e., pulmonary siderosis). Workers involved in the surface mining of
iron ore, crushing and milling for transport, or smelting the ore into
elemental iron for steel manufacture may be exposed to iron dust. The pure iron
oxide probably causes little lung injury or fibrosis, but substantial amounts of
silica and other silicates may be mixed in the iron ore. These fibrogenic
contaminants are prob- ably responsible for the lung disease that may result.
