What is the pathophysiology of smoke inhalation caused by zinc oxide?

Updated: Oct 15, 2021
  • Author: Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS  more...
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Zinc oxide is a constituent of HC smoke, also termed "white smoke," which was developed by the French and US Chemical Warfare Service after World War I. A number of reports have been published on various lung abnormalities occurring in military personnel and firefighters exposed to smoke from HC smoke bombs during training drills.

HC smoke is created by combustion of a mixture of equal amounts of hexachloroethane, zinc oxide, and approximately 7% grained aluminum or aluminum powder. When ignited, these release zinc chloride, and the pyrotechnic mixture of zinc chloride and hexachloroethane rapidly absorbs moisture from the air to form a grayish white smoke.

Other chemicals also are released in the combustion process, such as chlorinated hydrocarbons (eg, phosgene and carbon tetrachloride), chlorine gas, CO, and several other compounds. These most likely contribute to the observed respiratory effects.

HC has a sweetish acrid odor, even at moderate concentrations. HC exposure can produce a gradual decrease in total lung capacity, vital capacity, and diffusion capacity of carbon monoxide (DLCO). It also is associated with the development of pulmonary edema, increased airway resistance, and decreased compliance. These changes were found to be reversible with cessation of episodic exposure. [17]

While upper respiratory tract damage can occur from HC, the mean diameter of the primary smoke particles is approximately 0.1 micrometers, allowing them to reach the alveoli. In a retrospective cohort study of 20 patients, Hsu et al reported significant impairment of pulmonary function within 3-21 days following acute exposure. [18] Follow up in 1-2 months showed significant improvement with mild-to-moderate exposures, whereas severe exposures led to interstitial fibrosis and continued functional limitation.

In a study by Conner et al performed with guinea pigs, exposure to ultrafine HC particles (0.05 µm) in increasing degrees was associated with a dose-response elevation in protein, neutrophils, and angiotensin-converting enzyme found in lavage fluid. [19] A direct relationship also was observed with alkaline phosphatase, acid phosphatase, and lactate dehydrogenase in lavage fluid. Centriacinar inflammation was seen histologically, indicating evidence of pulmonary damage.

An interesting study by Marrs et al involving mice, rats, and guinea pigs demonstrated a positive association of alveologenic carcinoma in a dose-response trend to HC smoke as well as a variety of inflammatory changes. [20] These researchers concluded that hexachloroethane and zinc, as well as carbon tetrachloride (which may be present in HC smoke), may be animal carcinogens in certain circumstances. This raises the suspicion of HC as a potential human carcinogen.

Hepatotoxicity has also been described in humans exposed to HC smokes in enclosed spaces during military training. [21] The toxic effects appear to be primarily due to the chlorinated compounds produced by combustion: tetrachloromethane, tetrachloroethylene, hexachlorobenzene, and carbon tetrachloride. This last compound is well known for its hepatotoxicity. Acute exposure causes elevated liver enzyme levels by day 1 or 2, with a peak around day 18-21. Liver function test results should normalize by 6 weeks.

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