Lymphatic transport of inhaled diesel particles in the lungs of rats and guinea pigs exposed to diluted diesel exhaust

Vostal, Jaroslav J.; Chan, Tai L.; Garg, Bindu; Lee, P.S.; Strom, Kenneth A.

doi:10.1016/0160-4120(81)90080-5

Cited by 10 publications

(2 citation statements)

References 13 publications

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“…Studies on diesel exhaust exposure of rats have demonstrated that not all diesel exhaust particle (DP) containing macrophages leave the lung (Garg, 1983;Strom and Garg, 1981;White and Garg, 1981;Vostal et al, 1980;Wolff et al, 1987). Aggregations of DP-laden cells are observed as macroscopic maculation on gross lung specimens.…”

Section: Introductionmentioning

confidence: 96%

Inhaled particle retention in rats receiving low exposures of diesel exhaust

Strom¹,

Garg²,

Johnson³

et al. 1990

Journal of Toxicology and Environmental Health

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To study the effects of a low concentration exposure on the retention and clearance of submicron particles from the lungs, we exposed male Fisher 344 rats to diesel exhaust diluted to 50 micrograms diesel exhaust particles (DP)/m3, 20 h/d, 7 d/wk for 52 wk. Lung burdens (amount of DP in lungs) and the alveolar macrophage burdens were measured up to 52 wk postexposure. By 1 yr postexposure at least 80% of the DP was eliminated from the lungs and similarly cleared from the lavaged pool of macrophages. The DP remaining in the lungs was observed in alveolar, parabronchial and paravascular maculae. In contrast to previous high concentration exposure studies, only trace amounts of particles were observed in the mediastinal lymph nodes. To study the concentration dependence of particle retention, rats were exposed to equivalent exposures of 18 d x mg DP/m3 delivered at 5700 micrograms/m3 for 3 d, 1600 micrograms/m3 for 12 d, 250 micrograms/m3 for 72 d, or 50 micrograms/m3 for 365 d. Higher lung and macrophage burdens were initially achieved with the brief, high concentration exposures. During the postexposure period, animals exposed to the higher concentrations cleared more of the lung burden. Exposure to lower concentrations resulted in higher long-term lung burdens. These results are consistent with a model of lung clearance in which the macrophage burden and the duration of exposure are both important to the formation of the maculae. In a brief high concentration exposure, the macrophage burden rises rapidly, but then declines rapidly. However, in longer low concentration exposures, the macrophage burden will not reach the same peak, but stays at intermediate levels during the exposure and stimulates a steady development of the lung maculae from particle-laden macrophages leaving the active pool of pulmonary phagocytes.

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Section: Introductionmentioning

confidence: 96%

Inhaled particle retention in rats receiving low exposures of diesel exhaust

Strom¹,

Garg²,

Johnson³

et al. 1990

Journal of Toxicology and Environmental Health

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“…One of the primary defense mechanisms for clearance of particulates from the lower respiratory tract is the pulmonary alveolar macrophage (PAM). These ceils phagocytize particulates inhaled into the lower airways and subsequently such particulates are cleared by mucociliary transport and expectoration or by the pulmonary lymphatic system (Vostal et al, 1980). The physical properties of particulates such as silica and asbestos pose a problem in clearance by macrophages.…”

mentioning

confidence: 99%

In vitro cytotoxicity of chrysotile asbestos to human pulmonary alveolar macrophages is decreased by organosilane coating and surfactant

et al. 1986

Cell Biol Toxicol

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Human pulmonary alveolar macrophages were used to quantitate the cytotoxic effect of surface-altered chrysotile asbestos. Little difference was observed in mortality between chrysotile asbestos that was surface-treated to a 42% extent by a hydrophobic organosilane or untreated chrysotile. Little or no effect on mortality was observed when human pulmonary alveolar macrophages were cultured with untreated chrysotile or acid-leached asbestos in the presence of 10 mM dipalmitoyl lecithin. However, when human pulmonary alveolar macrophages were cultured with a hydrophobically-treated (to a 42% or 95% extent) chrysotile asbestos in the presence of 10 mM dipalmitoyl lecithin, a statistically significant decrease in mortality was observed compared to untreated chrysotile. No mutagenic activity was observed when V79 cells were cultured with acid-leached, or 42% hydrophobically-treated chrysotile asbestos, even when human pulmonary alveolar macrophages were included as an activation source. The 95% hydrophobically-treated and acid-leached chrysotile also exhibited decreased binding of benzo[a]pyrene compared to untreated chrysotile asbestos.

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Early pulmonary response of the rat lung to inhalation of high concentration of diesel particles

White

Garg

1981

J of Applied Toxicology

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Light microscopy was used to study the pathologic alterations in the rat lung after timed diesel exposures to 6000 micrograms m-3 of diesel particulates ranging from 6 h to 9 weeks. As a general reaction, an increase in alveolar macrophages containing diesel particles, an increase in type II pneumocytes, and an accumulation of inflammatory cells within the alveoli and septal walls was observed. Histochemical differentiation between type II cells and alveolar macrophages was clearly delineated by the use of the PAS (periodic acid Schiff) stain in which macrophages stained positive and type II cells negative for this reaction. After the 9-week exposure, the accumulation of macrophages and accompanying type II cell reaction resulted in the formation of alveolar complexes that seemed to be preferentially localized near the terminal bronchioles. The similarity of the lesion to that of 'macrophage alveolitis' produced in animals repeatedly exposed to coal dust is emphasized, although the ultimate clinical significance of the complex formation cannot be assessed within the time limits of the experimental observation.

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Lymphatic transport of inhaled diesel particles in the lungs of rats and guinea pigs exposed to diluted diesel exhaust

Cited by 10 publications

References 13 publications

Inhaled particle retention in rats receiving low exposures of diesel exhaust

Inhaled particle retention in rats receiving low exposures of diesel exhaust

In vitro cytotoxicity of chrysotile asbestos to human pulmonary alveolar macrophages is decreased by organosilane coating and surfactant

Early pulmonary response of the rat lung to inhalation of high concentration of diesel particles

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