Travels with Charlie

Immediate effects

The immediate effects of chlorine gas toxicity include acute inflammation of the conjunctivae, nose, pharynx, larynx, trachea, and bronchi. Irritation of the airway mucosa leads to local edema secondary to active arterial and capillary hyperemia. Plasma exudation results in filling the alveoli with edema fluid, resulting in pulmonary congestion.

Pathologic findings

Pathologic findings are nonspecific. They include severe pulmonary edema, pneumonia, hyaline membrane formation, multiple pulmonary thromboses, and ulcerative tracheobronchitis.

The hallmark of pulmonary injury associated with chlorine toxicity is pulmonary edema, manifested as hypoxia. Noncardiogenic pulmonary edema is thought to occur when there is a loss of pulmonary capillary integrity, and subsequent transudation of fluid into the alveolus is present. The onset can occur within minutes or hours, depending upon severity of exposure. Persistent hypoxemia is associated with a higher mortality rate.

The eye seldom is damaged severely by chlorine gas toxicity; however, burns and corneal abrasions have occurred. Acids formed by the chlorine gas reaction with the conjunctival mucous membranes are buffered, in part, by the tear film and the proteins present in tears. Consequently, acid burns to the eye typically cause epithelial and basement membrane damage but rarely damage deep endothelial cells. Acid burns to the periphery of the cornea and conjunctiva often heal uneventfully, while burns to the center of the cornea may lead to corneal ulcer formation and subsequent scarring.

In animal models of chlorine gas toxicity, immediate respiratory arrest occurs at 2000 ppm, with the lethal concentration for 50% of exposed animals in the range of 800-1000 ppm. Bronchial constriction occurs in the 200-ppm range with evidence of effects on ciliary activity at exposure levels as low as 18 ppm. With acute exposures of 50 ppm and subacute inhalation as low as 9 ppm, chemical pneumonitis and bronchiolitis obliterans have been noted. Mild focal irritation of the nose and trachea without lower respiratory effects occur at 2 ppm.

In one study of chlorine gas toxicity conducted on human volunteers, 4 hours of exposure to chlorine at 1 ppm produced significant decreases in forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and peak expiratory flow rate. An increase in airway resistance was demonstrated. In a controlled volunteer study, patients with hyperreactive airways demonstrated an exaggerated airway response to exposure of 1 ppm chlorine gas. While in another study, patients with rhinitis and advanced age demonstrated a significantly greater nasal mucosal congestive response to chlorine gas challenge than patients who did not have rhinitis or those of younger age. However, the mechanism of response to chlorine in nasal tissue does not appear to include mast cell degranulation.