Respiratory effects of sulfur mustard exposure, similarities and differences with asthma and COPD

Previous research has found relationships between sulfur mustard (SM) toxicity and its adverse effects.

SM is highly toxic to the respiratory system, leading to hacking cough, rhinorrheachest tightness, acute pharyngitis and laryngitis, chronic bronchitis and lung fibrosis. In this review, based on the scientific literature, we provide an updated summary of information on SM exposures and their differences with asthma and COPD.

Information of this review was obtained by searching Medline/PubMed, ScienceDirect, Scopus, Google Scholar, ISI Web of Knowledge and Chemical Abstracts.

SM exposure can decrease pulmonary function tests (PFTs) values. In addition, inflammatory cell accumulation in the respiratory tract and increased expression of some pro-inflammatory cytokines including tumor necrosis factor-α (TNFα), IL-1a, IL-1β, and reactive oxygen radicals due to SM exposure have been shown. Matrix metalloproteinase (MMP) which degrade extracellular matrix proteins, contributing to inflammatory cell recruitment, tissue injury and fibrosis are also up-regulated in the lung after SM exposure. In the lung, SM exposure also can cause serious pathological changes including airway inflammation, parenchymal tissue destruction and airway obstruction which can lead to asthma or chronic obstructive pulmonary disease (COPD). Following SM poisoning, DNA damage, apoptosis and autophagy are observed in the lung along with the increased expression of activated caspases and DNA repair enzymes.

In the present article, respiratory symptoms, changes in PFTs, lung pathology and lung inflammation due to SM exposure and the similarities and differences between them and those observed in asthma and COPD were reviewed.