Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.


The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Your Environment. Your Health.

Publication Detail

Title: The Role of Iraqi Dust in Inducing Lung Injury in United States Soldiers-An Interdisciplinary Study.

Authors: Harrington, Andrea D; Schmidt, Millicent P; Szema, Anthony M; Galdanes, Karen; Tsirka, Stella E; Gordon, Terry; Schoonen, Martin A A

Published In Geohealth, (2017 Jul)

Abstract: United States soldiers are returning from the Greater Middle East with respiratory illnesses ranging from new onset asthma to constrictive bronchiolitis. The etiology of the diseases is unknown. A study was conducted to determine the possible role of local mineral dust in the development of abnormal respiratory illnesses in soldiers during and after deployment in Iraq. A dust sample obtained in proximity to a burn pit in Camp Victory, Iraq, (CVD) was characterized both chemically and mineralogically. For comparison, a dust sample from Fort Irwin, California, (FID) was also collected. The ability of the dust samples to generate reactive oxygen species (ROS) was quantified, as well as their ability to generate an inflammatory stress response (ISR) in human lung epithelial cells. Both samples are comprised of common silicate and carbonate minerals and contain heavy metals with concentration ranges expected for mineral dust. The ISR generated by each sample was within the range of inert material with the minimal stress generated associated with the carbonate phases. The findings based on this one sample suggest that the origin of the disease is not driven by the particles ability to generate ROS. However it is likely that particle overload, and associated complications, or endotoxin contribute extensively to pathogenesis.

PubMed ID: 29085918 Exiting the NIEHS site

MeSH Terms: No MeSH terms associated with this publication

to Top