Elsevier

Toxicology

Volume 99, Issue 3, 23 May 1995, Pages 153-167
Toxicology

Biological effects of diesel exhaust particles (DEP). II. Acute toxicity of DEP introduced into lung by intratracheal instillation

https://doi.org/10.1016/0300-483X(94)03013-RGet rights and content

Abstract

Histopathological examination and cytological analyses in bronchial alveolar lavage fluids (BALF) were performed to clarify the acute toxicity of diesel exhaust particles (DEP) introduced into the lung of ICR mice by intratracheal instillation. Activated charcoal (Norit) was intratracheally administered as a control for non-oedemagenic carbon particles. After administration of two doses (0.4 mg or 0.8 mg per mouse) of DEP, lung water contents increased with instillation dose and with time and increased 1.9 and 2.7-fold, respectively, compared to control animals 24 h after the administration of DEP. In contrast, the instillation of Norit had no effect on the increase in water contents. An inflammatory response in lungs was observed by an increase of inflammatory cells in BALF from mice instilled with DEP. The degree of increase in neutrophils of BALF from mice treated with DEP was much greater than in mice treated with Norit. An intense color of MB-pigment, which showed the extent and degree of endothelial cell injury, was found up to 4 h after administration of DEP. Histopathologically, the disruption of capillary endothelial cells, the detachment from their basement membrane and necrosis, disruption and desquamation of type I pneumocytes were observed, 6 h after the injection of DEP, by electron microscopy. An influx of neutrophils into alveoli, intra-alveolar hemorrhage, perivascular oedema and bronchiolar cell hypertrophy were detected between 18 and 24 h after DEP administration. However, the magnitude of these appearances was greater in mice treated with 0.8 mg of DEP than in mice treated with 0.4 mg. The administration of Norit caused an increase of alveolar macrophages and slight infiltration of neutrophils into the alveolar air spaces and alveolar septa in the animals and had no effects on the bronchioles. These results may suggest that damage of capillary endothelial cells and type I pneumocytes are the earliest changes of lung toxicities by DEP and these cell injuries lead to alveolar oedema and the subsequent inflammatory response.

References (43)

  • G. Vogl et al.

    Diesel soot particles catalyze the production of oxyradicals

    Toxicol. Lett.

    (1989)
  • I.Y.R. Adamson et al.

    Endothelial injury and repair in radiation-induced pulmonary fibrosis

    Am. J. Pathol.

    (1983)
  • J.D. Crapo et al.

    Structual and biochemical changes in rat lungs occurring during exposures to lethal and adaptive doses of oxygen

    Am. Rev. Respir. Dis.

    (1980)
  • N.R. DiLuzio

    Antioxidants, lipid peroxidation and chemical-induced liver injury

  • M.A. Fox et al.

    Photoxidation of anthracene on atmospheric particulate matter

    Science

    (1979)
  • R.B. Fox et al.

    Prevention of thiourea-induced pulmonary oedema by hydroxyl radical scavengers

    J. Appl. Physiol.

    (1983)
  • T. Handa et al.

    Detection and average content levels of carcinogenic and mutagenic compounds from the particulates on diesel and gasoline engine mufflers

    Environ. Int.

    (1983)
  • U. Heinrich et al.

    Chronic effects on the respiratory tract of hamsters, mice and rats after longterm inhalation of high concentrations of filtered and unfiltered diesel engine emissions

    J. Appl. Toxicol.

    (1986)
  • U. Heinrich

    Carcinogenic effects of solid panicles

  • R.F. Henderson et al.

    Accumulation of diesel soot in lungs of rodents exposed in life span studies to diluted diesel exhaust

  • R.F. Henderson et al.

    Response of the lung to instilled versus inhaled panicles

  • Cited by (0)

    View full text