Pneumoconiosis refers to any nonmalignant chronic lung disease
resulting from inhalation and deposition of mineral, metallic, or
dust particles in the pulmonary interstitium. The most common agents
responsible for pneumoconioses are asbestos, silica, and coal. The
effect of these agents is dependent on the intensity and duration
of exposure as well as their clearance after deposition in the lung
- • A careful occupational and environmental history
of past inhalational exposures.
- • Evidence of pleural disease and/or interstitial
lung disease (especially bilateral reticular infiltrates).
Asbestos is a group of naturally occurring fibrous magnesium
silicates that are ubiquitous throughout the world. There are six
types of asbestos; one is serpentine (chrysotile) and five are fibrous
amphiboles (amosite, crocidolite, anthophyllite, tremolite, and
actinolite). Most disease results from direct or indirect exposure
to asbestos-containing materials during mining, milling, manufacturing,
installation, or removal of asbestos-containing products. Increased
risk among workers is not generally observed until at least 20 years
following initial exposure. However, patients with particularly
high levels of exposure may develop clinically evident disease within
10 years. The three major categories of asbestos-related disease
are asbestosis, asbestos-induced pleural disease, and cancer. Asbestosis
is parenchymal lung fibrosis that results from asbestos exposure.
As with coal workers’ pneumoconiosis and silicosis, the
degree of fibrosis is related to the amount and duration of exposure.
Typical asbestos fibers found in the lungs are 20–50 μm
in length. They deposit initially at bifurcations of conducting
airways and in alveoli. Fibers greater than 3 μm
in diameter generally do not penetrate the distal lung, but those
with diameters less than 3 μm readily translocate
into the interstitium and pleural space. Fibers greater than 5 μm
in length tend to be incompletely phagocytosed and are retained
in tissues where they initiate and sustain cellular and molecular
events that result in fibrogenesis. Asbestos triggers a chronic inflammatory
process promoted by oxidative injury and profibrotic growth factors
and cytokines. The principal determinants of the rate of disease
progression are cumulative dose, fiber type, and individual susceptibility.
The most significant preventive intervention in patients with
asbestosis is smoking cessation. Cigarette smoking in asbestos workers
increases the prevalence of radiographic pleuroparenchymal changes
and markedly increases the incidence of lung carcinoma.
Additional preventive measures include limiting exposure to asbestos.
The Occupational Safety and Health Administration (OSHA) has developed
regulations to control exposure in the workplace. Similar regulations
have also been developed by the Mine Safety and Health Administration
(MSHA) regarding exposure of miners. These regulations require use
of approved protective equipment, such as respirators, and recommended
work practices and safety procedures to limit exposure. Respiratory
protection requires that workers be issued the proper size and type
of mask, based on respirator fit testing procedures, and that they
be trained to recognize the hazards of ...