OVERVIEW OF INHALATION DISEASES
The inhalation of dusts and noxious gases into the lung may result in little damage or reaction if the agents have low biological activity or the exposure is minimal, but the results can be devastating injury, inflammation, or fibrosis if the agent is potent and carried by high dose or prolonged exposure. Virtually any fume, particle, or fiber that can be inhaled might cause a response in the lung if the material is in any way biologically active and the dose and exposure are sufficient.
Exposures to inorganic mineral dusts (e.g., silica,
asbestos, coal, mixed silicates) result in chronic lung diseases characterized
by fibrosis and distortion of tissue that produce progressive respiratory
impairment. These diseases generally progress slowly over time, often taking
decades from first exposure to clinical symptoms. The extent of disease depends
on the interaction between the intensity of exposure (airborne particle
load), the duration of exposure (cumulative dose), and the time since exposure
began. The key to control of these diseases is prevention by reducing the
levels of airborne dust in the workplace.
Many lung diseases caused by inhalation exposure to organic
or metal particulates are the result of a specific immune response.
Hypersensitivity pneumonitis (prototype, farmer’s lung disease), chronic
beryllium disease, cobalt pneumoconiosis (hard metal disease), and others only
appear after sensitization and the development of highly immunospecific
cell-mediated and humoral immune responses. In contrast to the pneumoconioses
caused by inorganic dusts and fibers, these diseases usually do not require a
high level of exposure to trigger them. After being sensitized, individuals may
respond intensely to very low ambient levels of the offending agent and may
become symptom free if exposure can be avoided. There is great variation among individuals,
and only a minority of those exposed may develop disease. In some instances
(e.g., beryllium), the disease may progress for years after the exposure ends. Brief
episodes of disease caused by immune responses to inhaled materials may clear
and leave no permanent lung damage, but repeated episodes or prolonged exposure
may result in end-stage fibrosis and severe respiratory impairment.
Toxic gases and fumes, smoke from fires, and volatile
chemicals used in industrial processes can cause injury to the lung when they
are inhaled. In most instances, these reactions are acute, occurring within
seconds to 48 hours of inhalation. If the injury is mild, complete resolution
without permanent impairment can be expected; if the injury is more severe,
then repair may be incomplete and may involve scarring. The speed and extent of
injury from inhaled gases depends on the biologic reactivity of the chemical
and its solubility in the water-based mucus that lines the lung. For example,
whereas highly soluble compounds, such as hydrochloric acid (HCl), dissolve
readily in mucus and cause injury primarily to the upper airway and larger bronchial
airways, relatively less soluble compounds, such as nitrogen dioxide (NO2),
produce damage primarily at the level of the alveoli and small airways. Intense
exposure to highly irritating fumes (e.g., chlorine gas, smoke) may cause an
instant response in the larynx, producing glottic closure and limiting more
distal damage at the expense of respiration.
Specific syndromes with both respiratory and systemic
symptoms can occur after inhalation exposures.
Metal fume fever is seen in welders and other workers
who heat zinc, copper, and other metals to high temperatures, generating fumes
and small respirable particles. Symptoms of metal fume fever occur 4 to 8 hours
after exposure and consist of an influenza-like illness with fever to 40˚C,
chills, headache, cough, sore throat, shortness of breath, nausea, muscle
aches, and malaise. The illness is self-limited and usually clears within 24 to
48 hours of its onset. It is believed to be caused by both the direct
irritation of the respiratory tract and the absorption of the metal into the
systemic circulation. Organic dust toxic syndrome (ODTS) is a form of inhalation
fever that results from exposure to aerosolized endotoxin (bacterial cell wall products),
glucans (fungal cell wall products), and related compounds. A flulike illness
develops 4 to 8 hours after exposure, with fever, muscle aches, malaise, cough,
shortness of breath, and sometimes wheezing. Exposures can occur in a wide
variety of settings, such as swine confinement facilities, sewage treatment
plants, cotton processing gins, grain storage silos, and grain milling
facilities. In patients with metal fume fever, ODTS, and other inhalation
fevers, tolerance may occur if exposure is frequent, with loss of tolerance
after an exposure holiday. Daily exposure may cause chronic bronchitis.
