Toxic Pneumonitis

Exposure: Industrial Spills, Fires, and Confined Space Accidents

"Short-term exposures to high concentrations of noxious gases, fumes, or mists generally are a result of industrial or transportation accidents or fires." [LaDou, p. 312)

Mechanism: Direct Cellular Injury

Acute toxic pneumonitis is caused by acute irritant injury and also by several other mechanisms: heavy metal pneumonitis, hydrocarbon aspiration, paraquat lung injury, and inhalation fever. [Murray, p. 1824] 

"The site of deposition of an inhaled gas is determined primarily by its water solubility, but also by the duration of exposure and minute ventilation of the victim.  [Sullivan, p. 224]

"Respirable particles with diameters in the 0.3-0.5 um range can bypass the upper airways and deposit in the more distal airways and alveoli. The clinical consequences of these injuries include diffuse bronchiolar inflammation and obstruction as well as alveolar filling (pulmonary edema). [Rosenstock, p. 333]

Toxic Inhalation Hazard (TIH)    "Term used to describe gases and volatile liquids that are toxic when inhaled." [ERG 2012]

The mechanism of toxicity after inhalation of a material includes:

Simple asphyxia (nitogen and methane)

Tissue asphyxia (carbon monoxide, cyanide, and hydrogen sulfide)

Nonrespiratory effects (hydrocarbon solvents and lead)

Stimulation of physiological responses (formaldehyde, sulfur dioxide)

Direct cellular injury (ammonia, chlorine, nitrogen dioxide, and phosgene) [Sullivan, Table 17-1]

"In acute pulmonary injury from inhaled irritants, exposure is typically brief and intense; initial symptom onset occurs within minutes to 24-48 hours after exposure. . . . Any irritant (high or low solubility) can cause pulmonary edema after sufficient exposure. . . . Heavy metal pneumonitis is clinically similar to irritant inhalation injury. As with low solubility gases, upper-airway mucous membrane irritation is minimal; thus, the exposure may have poor warning properties. Offending agents include cadmium, mercury, and in limited industrial settings, nickel carbonyl." [Olson, p. 530]  

"Some agrichemicals may cause toxic pneumonitis after non-inhalatory exposure. The best known of these agents is the herbicide paraquat which gains access to the lung via the circulation after gastrointestinal or (rarely) dermal absorption, and exerts a selective toxicity for the pulmonary epithelium." [Hendrick, p. 208]

Cause: Many Corrosive Gases and Vapors Plus Metal Fumes and Low-Solubility Gases (Phosgene, Ozone, and NO2)

In addition to cadmium and mercury, other metals (antimony, manganese, and beryllium) have been reported as causes of acute pneumonitis, but in the last 50 years there have been few reports to document such disorders. [Murray, p. 1827]

The major irritant airborne toxicants are ammonia (making plastics and fertilizer), bromine (making specialty chemicals), chlorine (plastics industry and water treatment), chlorine dioxide (making paper and food preparation), diborane (microelectronics), ethylene oxide (gas sterilizing), formaldehyde (embalmers, hospital workers, and making home furnishings and building materials), hydrogen chloride (chemical industry and firefighters), hydrogen fluoride (plastics and microelectronics), methyl isocyanate (pesticide manufacturing), nitrogen dioxide (welding and agriculture), ozone (arc welding, textile, and printing), phosgene (making isocyanates and pesticides and welding), sulfur dioxide (petroleum refining, smelting, making paper, and refrigeration). [LaDou, Table 30-4]

Effects: Non-Cardiogenic Pulmonary Edema

 The potential effects of inhaled irritants include irritation (eyes, nose, and throat), laryngeal edema (upper airway), tracheobronchitis (lower airway), and pneumonitis/pulmonary edema/adult respiratory distress syndrome (lung parenchyma). [LaDou, Table 20-2]

In this chapter, toxic pneumonitis refers to acute or subacute disorders of chemically induced injury in the lung parenchyma. . . . many agents that can cause toxic tracheo-bronchitis may also cause toxic pneumonitis, and some overlap is inevitable among disease descriptions." [Hendrick, p. 201]

Disease Definition in Haz-Map

In this database, agents linked to toxic pneumonitis are divided into two categories: primary and secondary. The primary chemicals can cause acute pneumonitis in animal experiments and are listed as toxic inhalation hazards (TIH) or releasers of TIH gases when spilled in water according to the 2012 Emergency Response Guidebook. These chemicals are linked to the occupational disease "Pneumonitis, toxic." The secondary chemicals are not linked to the occupational disease, but they are tagged with "Toxic Pneumonitis" as an adverse effect. Because of their importance in work-related exposures, cadmium fume, welding fumes, ozone, and elemental mercury vapor are also linked to the occupational disease even though they are not designated TIH. Also, all chemicals in the category "Corrosive Gases" are linked to the occupational disease.



Revised: January 09, 2013

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