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Comparison of pulmonary response to inhaled and intratracheally instilled diesel exhaust particulate.

Al-Humadi-NH; Siegel-PD
Toxicologist 2000 Mar; 54(1):14
Diesel exhaust particulate (DEP) is a complex mixture of polyaromatic hydrocarbons, ash, transition metals, and carbon core. Exposure levels of DEP up to 2 mwm3 has been documented in underground mines, railroad, construction, and auto repair industries. Such exposures have been associated with pulmonary inflammation, fibrosis, lung cancer, increased rate of respiratory infections and enhanced allergic sensitization. The purpose of this study was to compare the effect of the inhaled (4hr exposure, 17mg/m3) and intratracheally instilled (IT) DEP (5mg/kg b. wt.) and carbon black (CB, 34 mg/m3) particulate on pulmonary inflammation, pulmonary associated lymph node cells (LNC) and alveolar macrophages (AM) in a Brown Norway rat model. Carbon black was used as a surrogate of the non-extractable carbon core of DEP. Cellular Cysteine (CYS) and glutathione (GSH) levels were analyzed by conjugation to monobromobimane and subsequent HPLC-fluorescent analysis. Alveolar macrophage IL-1 and TNF-production were also assessed three days post exposure. Both, DEP and CB were generated by nebulizing suspended particles through a diffusion dryer into a nose-only chamber. Greater than 90% of the particles generated were in the submicron range. The microscopic evaluation of the DEP and CB particulate revealed similarities in shape and size between them. Inhaled DEP caused a significant increase in the levels of glutathione and cysteine in the LNC, but not AM. LNC thiols were unchaged following IT DEP, but AM GSH was elevated. A significant decrease of AM TNF- of DEP exposed rats after ex vivo endotoxin challenge was also observed in both IT and inhalation groups. Instillation of DEP caused pulmonary inflammation as noted by the increases in neutrophils count, and lavage protein and LDH levels. Inhaled DEP did not produce measurable pulmonary inflammation. The cause of the differences observed between acute inhalation vs IT DEP in pulmonary inflammation and thiol content is not known, but may be due to done deposited in the lung.
Particulates; Diesel-exhausts; Pulmonary-system-disorders; Respiratory-system-disorders; Polychlorinated-aromatic-hydrocarbons; Exposure-levels; Fibrosis; Lung-cancer; Sensitization; Underground-mining; Construction-industry; Railroad-industry; Automotive-industry; Laboratory-animals; Animals; Animal-studies
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The Toxicologist. Society of Toxicology 39th Annual Meeting, March 19-23, 2000, Philadelphia, Pennsylvania