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mucous glands. The ciliated cells and the mucus serve as an escalator to move materials from the deep lung to the oral cavity where they are swallowed and excreted.

The conducting airways extend through the respiratory bronchioles, which terminate into the acini, consisting of alveolar ducts, alveolar sacs, alveoli and associated blood vessels, lymphatic tissues, supportive tissues, and nerve endings. The alveoli are the primary site of gas exchange with the blood, and are lined by two specialized types of epithelial cells (Type I and Type II alveolar epithelial cells). The total alveolar surface area in the adult human is about 100 m 2 during deep inspiration (Menzel and Amdur, 1986; Phalen and Prasad, 1988).

The most important type of inhalation exposure of the respiratory tract to sulfur mustard or Lewisite, including the chamber tests and field trials, has been to vapors of these compounds (Papirmeister et al., 1991). Inhaled vapors rapidly contact airway surfaces by the process of molecular diffusion (Lippmann, 1992). Surface uptake of the vapor then depends on the chemical properties of the inhaled compound. Highly reactive compounds with characteristics similar to sulfur mustard are generally removed higher in the respiratory tract and, thus, cause most of their damage in nasal, laryngeal and bronchial regions of the respiratory tract (Dahl, 1990; Dahl et al., 1991; Lippmann, 1992).

ACUTE EFFECTS AND BIOLOGICAL MECHANISMS

The inhalation of sulfur mustard or Lewisite causes acute damage to the respiratory tract, but the symptoms of exposure are not immediate and develop over a period of several days. Pulmonary injury is in fact the principal cause of mortality in the first few days to weeks after exposure to sulfur mustard (Hosseini et al., 1989; Papirmeister et al., 1991; Willems, 1989). The signs and symptoms of respiratory tract damage following inhalation of various levels of sulfur mustard are summarized in Table 7-1.

Damage to the respiratory tract involves acute edema (swelling), inflammation, and destruction of the airway epithelial lining. Depending on the dose, the destruction may be mild to severe. Severe damage includes destruction of the epithelium with subsequent formation of pseudomembranes (such as those formed in diphtheria infections), which may slough and obstruct the airway, resulting in death. In most cases, the injury is most severe in the larynx, trachea, and bronchi, with small bronchi less affected than large bronchi. The basement membranes that underlie the epithelium are edematous and are infiltrated by white blood cells. In some cases, presumably with high exposures, damage extends into the deeper alveolar regions, resulting in generalized edema of the lung. Finally, allergic hypersensitivity reactions to inhaled sulfur



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