Acute inhalation injury may result from frequent and widespread use of household cleaning agents and industrial gases (including chlorine and ammonia).
Irritant gases are those that, on inhalation, dissolve in the water of the respiratory tract mucosa and provoke an inflammatory response, usually from the release of acidic or alkaline radicals.
Depending on the type and amount of irritant gas inhaled, victims can experience symptoms ranging from minor respiratory discomfort to acute airway and lung injury and even death.
A common response cascade to a variety of irritant gases includes inflammation, edema and epithelial sloughing, which if left untreated can result in scar formation and pulmonary and airway remodeling.
The September 11 attacks in 2001 and forest fires in U.S. states such as California and Nevada are examples of incidents that have caused smoke inhalation injury.
The National Institute for Occupational Safety and Health recommends that a person wear splash proof goggles, a face shield and a respirator mask when working in the vicinity of chlorine gas.
With increased exposure, symptoms may progress to labored respirations, severe coughing, chest tightness, wheezing, dyspnea, and bronchospasm associated with a decrease in oxygen saturation level.
[10][11][citation needed] Phosgene, notably used as a chemical weapon during World War I, is also used as an industrial reagent and building block in synthesis of pharmaceuticals and other organic compounds.
[14] Ammonia is generally used in household cleaning products, as well as on farms and in some industrial and commercial locations, and this makes it easy for accidental or deliberate exposure to occur.
[18][19] This agent also causes respiratory tract lesions, bone marrow depression, and eye damage, the epithelial tissues of these organs being predominately affected.
Inhalation of high doses of this gas causes lesions in the larynx, trachea, and large bronchi with inflammatory reactions and necrosis.
A common exposure involves accidental mixing of household ammonia with cleansers containing bleach, causing the irritant gas monochloramine to be released.
More water-soluble gases (e.g. chlorine, ammonia, sulfur dioxide, hydrogen chloride) dissolve in the upper airway and immediately cause mucous membrane irritation, which may alert people to the need to escape the exposure.
Permanent damage to the upper respiratory tract, distal airways, and lung parenchyma occurs only if escape from the gas source is impeded.
[25] These agents are less likely to produce early warning signs (phosgene in low concentrations has a pleasant odor), are more likely to cause severe bronchiolitis, and often have a lag of ≥ 12 h before symptoms of pulmonary edema develop.
Fluid filled airspaces, loss of surfactant, microvascular thrombosis and disorganized repair (which leads to fibrosis) reduces resting lung volumes (decreased compliance), increasing ventilation-perfusion mismatch, right to left shunt and the work of breathing.
Prolonged inflammation and destruction of pneumocytes leads to fibroblastic proliferation, hyaline membrane formation, tracheal remodeling and lung fibrosis.
Ten to 14 days after acute exposure to some agents (e.g. ammonia, nitrogen oxides, sulfur dioxide, mercury), some patients develop bronchiolitis obliterans progressing to ARDS.
Bronchiolitis obliterans with organized pneumonia can ensue when granulation tissue accumulates in the terminal airways and alveolar ducts during the body's reparative process.
Hemorrhaging, signifying substantial damage to the lining of the airways and lungs, can occur with exposure to highly corrosive chemicals and may require additional medical interventions.
[36] Inhaled and systemic forms of β2-agonists used in the treatment of asthma and other commonly used medications, such as insulin, dopamine, and allopurinol have also been effective in reducing pulmonary edema in animal models but require further study.
A recent study documented in the AANA Journal discussed the use of volatile anesthetic agents, such as sevoflurane, to be used as a bronchodilator that lowered peak airway pressures and improved oxygenation.
Additional research must be directed at developing sensitive and specific tests to identify individuals quickly after they have been exposed to varying levels of chemicals toxic to the respiratory tract.
Given the constant threat of bioterrorist related events, there is an urgent need to develop pulmonary protective and reparative agents that can be used by first responders in a mass casualty setting.
[36] Other feasible routes of administration could be inhalation and perhaps to a lesser extent oral – swallowing can be difficult in many forms of injury especially if accompanied by secretions or if victim is nauseous.
Potential tissue reparative agents can be evaluated in vitro by determining their effects on stimulation of pulmonary and airway epithelial cell proliferation.