Toxic Inhalational Lung Injury

Chapter 56 Toxic Inhalational Lung Injury

A variety of chemicals, when liberated into the atmosphere as gases, fumes, or mist, can cause irritant lung injury or asphyxiation. As summarized in Table 56-1, any level of the respiratory tract can be the target for toxins, which produce a wide range of disorders, from tracheitis and bronchitis to pulmonary edema.

Table 56-1 Inhalational Toxins and Range of Toxicity

Toxins Effects
Ammonia Mucous membrane irritation and sloughing
Bronchiectasis, pulmonary interstitial fibrosis
Ammonia, phosgene, hydrogen sulfide Laryngeal edema and obstruction
Carbon monoxide, cyanide, hydrogen sulfide Asphyxiation
Chlorine, phosgene Acute respiratory distress syndrome
Hydrofluoric acid Systemic effects, hypocalcemia, hypomagnesemia
Hydrogen chloride, chlorine Tracheobronchitis
Hydrogen fluoride, mustard gas Chemical pneumonitis
Hydrogen sulfide Bacterial pneumonia
Nitric oxide Systemic effects, methemoglobinemia
Oxides of nitrogen, sulfur oxides Obliterative bronchiolitis (bronchiolitis obliterans)
Sulfur dioxide, hydrogen chloride, oxides of nitrogen, ozone Bronchoconstriction, airway edema, asthma

Etiology and Risk Factors

Major risk factors for inhalational exposure and injury are related to the environment and not to the individual. Exposures occur randomly in the general environment, such as when a chemical spill occurs on a highway or railroad, carbon monoxide (CO) leaks in a home, or a person incorrectly mixes household chemicals together and releases a gas or aerosol. Smoke that comprises the pyrolysis products of synthetic materials is a common cause of injury to the respiratory tract, as well as a cause of pulmonary insufficiency and death from fires.

Occupational injuries more often occur when workers handle chemicals, work in areas that are inadequately ventilated, or enter exposed areas with improper protective equipment. Table 56-2 lists sources of occupational exposure to major chemical causes of irritant lung injury and asphyxiation.

Table 56-2 Inhalational Toxins and Source of Exposure

Toxin Sources of Exposure
Ammonia Agriculture, explosives, plastics
Carbon monoxide Firefighters, smoke inhalation, smelters, miners, transportation, home furnaces
Chlorine Household cleaners, paper, textiles, sewage treatment, swimming pools
Hydrofluoric acid Fertilizers, insecticides, glass and ceramic etching, masonry, metalworking, pharmaceuticals, chemical manufacture
Hydrogen chloride Fertilizers, textiles, dyes, rubber manufacture
Hydrogen cyanide Metallurgy, electroplating, plastics, polyurethane manufacture
Hydrogen sulfide Metallurgy, chemical manufacture, wastewater treatment, natural gas and oil drilling, paper mills, coke ovens, rayon manufacture, rubber vulcanization
Mustard gas Chemical warfare
Oxides of nitrogen Air pollution, welding, hockey rinks, chemical and dye manufacture, agriculture
Ozone Welding, air pollution, high altitude, chemical manufacture
Phosgene Firefighters; paint strippers; chemical, pharmaceutical, and dye manufacturing; chemical warfare
Sulfur dioxide Air pollution, smelting, power plants, chemical manufacture, paper manufacture, food preparation

Factors that influence the acute effects of toxic chemicals include solubility, particle size, concentration, duration of exposure, chemical properties, and individual factors such as minute ventilation. The more water-soluble compounds dissolve in the upper respiratory tract and airways, whereas the less water-soluble agents tend to bypass the upper airway and affect peripheral airways and pulmonary parenchyma (Figure 56-1).


In general, the upper airway can be affected by most inhaled toxins, which result in edema of the nasal passage, posterior oropharynx, and larynx. In severe cases, mucous membrane ulceration and hemorrhage ensue. Toxins of low water solubility may reach the lung parenchyma without necessarily producing upper airway lesions. If breath holding, laryngospasm, and normal “scrubbing” activities of the nasopharynx fail to contain the exposure, lesions develop in the trachea and bronchi (e.g., paralysis of cilia, increased mucus production, goblet cell hyperplasia, injury to airway epithelium, epithelial denudation, exudation, submucosal hemorrhage, edema). Pseudomembranes may form along the trachea and bronchi, causing various degrees of bronchiolitis, bronchiolitis obliterans (Figure 56-2), and organizing pneumonia (Figure 56-3). Bronchiolitis has been associated with exposures to oxides of nitrogen—nitric oxide (NO), nitrogen dioxide (NO2), and nitrogen peroxide (N2O4)—as well as sulfur dioxide, ammonia, chlorine (Cl2), phosgene, fly ash that contains trichloroethylene (C2HCl3), ozone (O3), hydrogen sulfide, hydrogen fluoride (HF), metal oxide fumes, dusts (e.g., asbestos, silica, talc, grain dust), free-base cocaine, tobacco smoke, and fire smoke.

Parenchymal injury is less common than airway damage. When alveolar or interstitial injury occurs, both epithelial damage and endothelial damage are observed, resulting in alveolocapillary leak and the pathologic changes of adult respiratory distress syndrome (ARDS). Diffuse alveolar damage (DAD) is a common histologic pattern in acute interstitial lung disease caused by inhaled toxins. It is characterized by widespread, diffuse edema, epithelial necrosis and cell sloughing (with exudates that fill the alveolar spaces), and formation of hyaline membranes (Figure 56-4). Later, DAD may organize, which leads to proliferation of type II pneumonocytes, resorption of the hyaline membranes and exudates, and fibroblast proliferation. Long-term survivors of such parenchymal injury may fully recover or may have various degrees of permanent interstitial fibrosis.

Clinical Features and Diagnosis

Diagnosis should focus on the nature of the compound inhaled, the magnitude and duration of exposure, and the water solubility of the inhaled agent. Inhalational injury is suspected in those who have facial burns or inflamed nares. Headache and dizziness, along with chest pains and emesis, suggest systemic poisons (e.g., cyanide, H2S). Unconscious victims found in confined spaces are assumed to have received longer inhalational exposures than conscious ones because of the unprotected airways and concentrated exposures. Evidence of hoarseness, upper airway stridor, wheezing or rales, cough, and sputum production is assessed. Chest radiographs may show pulmonary edema, atelectasis, or infiltrates (Figure 56-5), although they are often negative early after exposure. Flow-volume loops are the most sensitive noninvasive indicators of upper and lower airway obstruction. Hypoxemia in the face of a normal arterial partial pressure of oxygen (PaO2) suggests CO toxicity. Carboxyhemoglobin levels are obtained for all fire and explosion victims. Metabolic acidosis may indicate cyanide or H2S intoxication.

In patients who have persistent symptoms months after exposure, bronchial provocation tests with methacholine may help assess whether the patient has reactive airway dysfunction syndrome. Computed tomography (CT) may help determine if permanent fibrotic changes have developed.

Jun 12, 2016 | Posted by in RESPIRATORY | Comments Off on Toxic Inhalational Lung Injury

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