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Journal Article

Citation

Christiani DC. New Engl. J. Med. 2019; ePub(ePub): ePub.

Affiliation

From the Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston.

Copyright

(Copyright © 2019, Massachusetts Medical Society)

DOI

10.1056/NEJMe1912032

PMID

31491071

Abstract

A number of environmental agents are known to cause acute or subacute inhalation injury to the lung parenchyma. Indeed, emergency response guidelines for medical personnel describe toxic inhalation pneumonitis as a heterogeneous group of chemically induced injuries to the lung parenchyma as well as to the upper respiratory tract. The manifestations of such injury depend on the characteristics (e.g., solubility, composition) and the amount of the toxic compound or compounds inhaled.1 Much of what we know about toxic inhalation syndromes derives from high levels of exposure in either occupational settings (e.g., exposure to metals, solvents, acids, bases, ozone, phosgene, or chlorine dioxide) or community settings where fires or accidents may occur (e.g., factory explosions, derailments of chemical-bearing train cars, and overexposure to household cleaning agents). Depending on the type of chemical agent and the amount of material inhaled, patients may experience symptoms ranging from minor respiratory tract discomfort to acute airway injury and damage to the parenchyma with pneumonitis, alveolar edema, respiratory failure, and death. A common pathophysiological pathway includes inflammation, edema of airways with epithelial sloughing, alveolar inflammation, and edema with hypoxemia...


Language: en

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