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Airway epithelial damage and release of inflammatory mediators in human lung parenchyma after sulfur mustard exposure

Laboratoire de Toxicologie Respiratoire, Centre d'Etudes du Bouchet (Defense Medical Research Center), 91710 Vert-Le-Petit, France

J-P Gascard

CNRS, ERS 566, Centre Chirurgical Marie Lannelongue, 133 Av. de la Résistance, 92350 Le Plessis-Robinson, France

S Delamanche

Laboratoire de Toxicologie Respiratoire, Centre d'Etudes du Bouchet (Defense Medical Research Center), 91710 Vert-Le-Petit, France

C Brink

CNRS, ERS 566, Centre Chirurgical Marie Lannelongue, 133 Av. de la Résistance, 92350 Le Plessis-Robinson, France

This study was performed to evaluate the morphological effects of sulfur mustard on human lung parenchyma in vitro and to measure the metabolites of arachidonic acid which are released during acute exposure to the alkylating agent. Histological analysis of the tissue following exposure to sulfur mustard for a period of 45 min at 10 mM revealed the presence of paranuclear vacuoles in the epithelium, specifically, in the ciliated cells. The release of metabolites of arachidonic acid were determined in the bath fluids by an enzymo-immunoassay. The basal release of prostaglandin E₂ (PGE₂:1.36±0.33 ng/g tissue) and 6- keto prostaglandin F₁ (6-keto PGF₁: 8.83±1.17 ng/g tissue) were not modified during tissue exposure to sulfur mustard (45 min, 0.1 mM). In addition, the basal release of cysteinyl-leukotriene E₄ (LTE₄: 1.55±0.44 ng/g tissue) was also not altered by challenge of the tissues with sulfur mustard. In contrast, when the human lung parenchyma was stimulated with anti human IgE (anti-IgE) only the basal release of the metabolite of the 5-lipoxygenase pathway was significantly increased (LTE₄: 6.84±1.57 ng/g tissue).

These data suggest that sulfur mustard may produce morphological alterations in epithelial cells and at the time point studied (45 min exposure), this effect is not associated with a release of arachidonic acid metabolites. However, the increased release of LTE₄ by anti-IgE suggests that the target cells for sulfur mustard and anti-IgE in the human lung may be different.

Key Words: SM • human lung parenchyma

Human & Experimental Toxicology, Vol. 18, No. 2, 77-81 (1999)
DOI: 10.1177/096032719901800203


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